Respiratory and Cardiovascular Systems, Blood Composition

Respiratory System
It is oxygen that is required to convert the stored fuel in the muscle tissue to useable energy, it is this conversion that produces carbon dioxide, and it is the respiratory system that provides both the intake of oxygen and the removal of carbon dioxide.

This system consists of a number of components they are:
The larynx or voice box
The trachea or windpipe
The alveoli, which are the small air sacs that make up the lung tissue

The larynx is made up of 9 pieces of interconnecting cartilage with muscles attached to each section that open or close the throat as required and allow the passage of air but not food or water.

While the trachea is a long flexible tube composed of rings of cartilage, (a bit like the old vacuum cleaner hose), this tube then branches out into progressively smaller tubes called the bronchial tubes.
At he end of which are the millions of small air sacs that make up the lungs (alveoli).
These small air sacks are surrounded by small capillaries and blood vessels that are directly connected to the main pulmonary blood vessels of the heart.

Respiratory System Functions
First of all it takes oxygen from the air and transfers it into the blood stream where it is taken up by the haemoglobin part of the red blood cells.
The only reason that oxygen is transferred from the air in the lungs to the haemoglobin is because the oxygen levels in the air being inhaled are higher than the oxygen levels in the bloodstream.

It should also be remembered that the same applies to any other substances that may be in the air that the Greyhound inhales into the lungs, such as carbon monoxide from car exhausts, or even viruses that may be suspended in tiny droplets of moisture in the air.

The second function is to remove carbon dioxide from the body; again this occurs due to the fact that the level of carbon dioxide in the blood is higher than in the air, so some simply transfers out of the bloodstream.

It is the brain that monitors the level of carbon dioxide and oxygen in the blood via special receptors in the main blood vessels to the heart and regulates the rate of breathing and thereby the rate of the carbon dioxide /oxygen exchange.

The receptors in the main blood vessels that measure the level of oxygen or carbon dioxide in the blood stream are not the only regulators of the breathing rate by the greyhound.

An increase in body temperature also increases the breathing rate, and it is the evaporation that occurs in the respiratory system because of this rapid breathing or panting that provides cooling of the body.

So the third function of the respiratory system is to provide for the cooling of the greyhounds body.

The fourth function of the respiratory system is to help maintain the pH of the blood, and it does this by expelling carbon dioxide as required.

The fifth function is in sound production; air enters the system via the nose or mouth and enters the larynx where it may be used for barking, growling or howling.

Hyperventilation
However excitement, anxiety or illness may also affect the rate of breathing, and in certain circumstances this may have a detrimental effect on the greyhounds metabolic system.
Such as the panting and hyperventilating the greyhound may do while waiting at a track for a race.

This may cause a condition known as Respiratory Alkalosis.

Respiratory alkalosis is any clinical condition where Carbon Dioxide removal by the lungs, exceeds its production by body tissues.

Respiratory alkalosis is relatively common in low-grade lung inflammation, such as kennel cough, or any condition that includes hyperventilation.

Greyhounds suffering pre-race stress syndrome may suffer from respiratory alkalosis as a result of excessive barking.
However, body defence mechanisms in the case of respiratory alkalosis are extremely efficient and the condition normally clears up quickly without treatment, unless of course the greyhound suffers further stress as a result of an excessively hard race or trial, or simply was not fit or healthy enough to do what it was asked to do.

The rate of breathing may also cause a condition known as Respiratory Acidosis.

Respiratory acidosis is any clinical condition where Carbon Dioxide production, exceeds the ability of the lungs to remove it.

Respiratory acidosis is not common, except in extremely severe lung infections or when lung function is depressed, either under anaesthetic or from inappropriate drug use.

Anatomically the respiratory system has some unique features that help it to function efficiently.

As mentioned earlier, the larynx consists of nine pieces of cartilage that have muscles attached to them that open and close the opening, permitting air passage, but not food or water.
Keep this fact in mind, when you consider the following scenario.

The greyhound has just run a race or trail; you get to the wash bay and hose the feet, legs etc. cool the dog down and now you go to give it a drink out of the hose, but as soon as it tries to drink it starts coughing.

Or you go to give it a drink and the dog refuses to drink, and you think to yourself, what wrong with this dog, surely it needs a drink of water after that run.

So you stick the hose in the side of the mouth and the dog coughs or almost chokes itself.

All that has happened, is that the heaving for air that the dog has done during and after the run has caused cramp in the muscles of the larynx, and it is locked open, so any water that that enters the mouth will go straight into the windpipe.

A large number of greyhounds are not capable of drinking any water immediately after a run for that reason, more so if the run was a hard one in relation to the greyhound’s current state of fitness.

When the greyhound breathes in the air travels down the trachea (windpipe) to the smaller bronchial tubes. An important feature is that these are surrounded by muscle tissue that involuntarily functions to enlarge or reduce the diameter of those tubes as required.

Another important feature of the bronchial tubes is that they are lined with cells that have hair like projections on their surface (cilia) that continually move in an upward and outward motion and in this way remove any dust, or the mucus that is produced by the respiratory system.

The production of excessive amounts of mucus by the respiratory system due to inflammation of the airways, just like the inhaling of any foreign substance like food or water, will immediately trigger the coughing reflex.

Inflammation of the airways will also trigger an increased rate of breathing due to the fact that inflammation and the subsequent build up of mucus, reduce the size of the bronchial tubes and thereby restrict the airflow.

Problems affecting the respiratory system
Enlarged tonsils
Repeated bouts of tonsillitis will cause a permanent enlargement of the tonsils and this may interfere with the Greyhounds breathing during running.

The symptoms may include a reduction in performance over distances exceeding 400 meters noticeable loud snorting breathing after a run and prolonged recovery time to normal breathing.
Treatment, surgical removal of the tonsils is advised.

Excessive soft palate
The palate is a flap of tissue that extends down of the roof of the mouth to the back of the throat and separates the back of the throat and the nasal passage.

This is a genetic defect and consists of a larger than normal palate that interferes with the passage of air into the larynx.

The symptoms may include a reduction in performance over distances exceeding 400 meters and noticeable loud breathing both during and after a run, as well as prolonged recovery time to normal breathing.
Treatment, surgical shortening of the palate is advised.

Exercise induced bronchial constriction
This is a contraction or spasm of the muscles of the bronchial tubes in response to physical exertion.

Normally the requirement for more oxygen causes the muscles around the bronchial tubes to relax allowing for a greater airflow to the lungs. In greyhounds suffering this condition the opposite occurs, in other words the muscles around the bronchial tubes tighten and constrict the airflow.

This condition may also include a swelling of the mucus membranes of the smaller airways and an increase in mucus production.

The symptoms include a reduction in performance over distances exceeding 300 meters and a dry intermittent husky cough immediately after the run that may persist for up to 4 hours after the run.

In most instances the cause appears to be stress induced as it mainly seems to affect those greyhounds that shake and tremble before a run and tighten all over in the muscle tissue.

While the recommended treatment is the dosing with drugs that dilate the bronchial tubes such as the drugs used to treat asthma, however this will only reduce the after the run coughing, as the rules of racing as well as the sophisticated swabbing procedures rule that out as far as pre-race use is concerned.

The other thing to keep in mind is that a greyhound with a heart condition will display the same or similar symptoms as a greyhound with exercise induced bronchial constriction.

The Cardiovascular System
The term "cardiovascular" simply refers to the heart and blood vessels that are the pump and tubing that circulate the blood through the body.

It is a system that is highly efficient at taking in oxygen at the lungs and transporting it throughout the whole body, as well as taking the waste products from the body's metabolism and delivering them to the appropriate organs for processing or excretion.

The circulatory system also carries the nutrients from the digestive system and distributes them to the cells to use as sources of energy.

The blood contains buffers that allow the body to rapidly neutralize the acids produced by intense exercise, that is, if it is capable of doing so within the current state of health and fitness of the body.

Hormones produced by the various glands are carried to where they are required, and finally the blood contains the defence mechanism that helps protect the body against all types of infections.

In other words, everything that affects the blood will affect the body in some way and everything that affects the body will affect the blood.

And that is why blood tests are the most powerful tool at the disposal of the greyhound trainer when he or she needs to determine the true state of health of the greyhound.

However, like any tool you need to know how to use it, therefore the value of the blood tests to the trainer totally depend on the ability of the trainer to order the appropriate blood tests, and on the ability of both the trainer and the Veterinarian to interpret and act on the results.

The heart is located in the chest between and below the lungs and weighs a little over 1% of the Greyhounds body weight, in other words a 32 Kg Greyhound has or should have a heart that weighs around 350 grams, or about three quarters of a pound.

Which is extremely large when compared to other breeds of dogs.

The heart is really a hollow muscle containing four separate chambers or compartments, the two chambers on the left side of the heart are connected by an opening containing a one-way valve, the two chambers on the right side of the heart are similarly connected to each other.

The upper chambers are called an ATRIUM the lower chambers are called VENTRICLES.

The manner in which the heart pumps blood is reasonably simple, blood enters the heart at the atrium, and passes trough a one-way valve into the ventricle.

The muscles of the ventricle start to contract, the one-way valve closes, the muscles of the ventricle reduce the size of the chamber and squeeze the blood out of that side of the heart into the blood vessels.

Each of the main blood vessels also have a one-way valve at the start of the blood vessel to assist that process as it stops the blood returning to the ventricle as it relaxes and opens up again.

This function of the heart also explains the names given to the chambers of the heart; an atrium is the name given to the front section of a hall where people collect prior to going into the main hall.

While the name ventricle simply describes a device for venting or pushing something out.

Each side of the heart has a completely separate function that includes delivering blood to a different part of the body.

The right side of the heart collects blood from all of the body tissues, and sends it to the lungs to collect oxygen and get rid of carbon dioxide.

For that reason the right side of the heart is called the venous side of the heart, in other words it receives the blood from the veins of the body.

The left side of the heart receives freshly oxygenated blood from the lungs and pumps it out to all the body tissues via a large blood vessel called the AORTA.

For that reason the left side of the heart is called the arterial side of the heart as it supplies blood to all the arteries of the body.

The Blood Vessels
If you followed a single red blood cell as it left the ventricle of the LEFT side of the heart it would take the following journey.

As it leaves the left ventricle it passes through the AORTIC valve into the AORTA, which is the largest blood vessel in the body.

The aorta then divides in to smaller arteries and our red blood cell travelling through these arteries then enters the smallest of the arteries called an ARTERIOLE.

The arterioles then divide into smaller blood vessels called CAPILLARIES, and it is in the capillaries that our red blood cell hands over the oxygen and collects carbon dioxide.

As it travels on its way through the capillaries they soon begin to unite to form tiny veins called VENULES, these in turn unite to form the larger veins and our red blood cell would find itself being tipped out into the RIGHT atrium of the heart.

From this point the journey would continue through the non-return valve into the right ventricle of the heart, from there it is pumped past the PULMONIC valve to the PULMONARY ARTERY and into the lungs, in the lungs it releases the carbon dioxide and collects a fresh lot of oxygen.

After leaving the lungs via the PULMONARY VEIN it would enter the LEFT ATRIUM pass down through the valve and would be back where it started the journey in the first place.

From the above description you probably would have noted two things.
Any blood vessel containing blood being pumped out of the heart is called an ARTERY.
Any blood vessel containing blood returning to the heart is called a VEIN.

That description is good and well for the oxygen and carbon dioxide parts of the blood flow, you say, but what about the nutrients from the digestive system, how do they get to the muscle tissue?

Good question, well there is a main branch off the AORTA, this branch, via a system of arteries, supplies blood to the capillaries of the stomach and intestines, and is called the PORTAL system.

From there the blood containing the nutrients absorbed from the BOWEL WALL is transported to the liver via the PORTAL VEIN.

The liver being the main processing plant for the absorbed nutrients converts many of these to a type more suitable for use by the cells of the body.

The blood then leaves the liver via the HEPATIC vein which branches into the main vein entering the RIGHT atrium of the heart.

In other words, the nutrients required by the body are added to the blood stream just before the blood is pumped to the lungs for re-oxygenation.

The circulation of the blood depends entirely on the pumping action of the heart and involves a series of events that must be carefully coordinated.

During running and exercising the heart must beat more forcefully and the capillaries supplying the muscle tissue open up and bring in more blood at a time of peak demand.

At the same time the capillaries of the stomach and intestines partially close down to allow the shunting of blood to the areas where it is needed the most.

All of these various actions occur without any conscious control by the greyhound, as all of the muscles involved are non-voluntary muscles under the control of the AUTONOMIC nervous system.

This part of the nervous system maintains all of the body functions that are required to keep the greyhound alive and functioning.

It is also the AUTONOMIC nervous system that speeds up the heart rate during times of fear or excitement and triggers the release of blood glucose to stimulate muscle function and adrenaline to speed up reaction time as well as relaxing the heart rate during sleep or rest.

The number of times the heart muscle contracts per minute and pumps blood out to the body can be counted by placing one's fingers over an artery, it is called the heart rate.

If a greyhound has any weakness in the pumping action of the heart, or any leaking of the heart valves, there will be a reduction in the supply of oxygen to the muscles and the body in general.
As a result of the lack of oxygen there will be a reduction in the performance.

Such greyhound will often look perfectly healthy and fit, however they will fade dramatically towards the end of a run and gasp for air at the conclusion.

In severe cases they may stagger in the catching pen and turn a blue colour in the tongue or mouth membranes, with a breathing recovery rate that may take 30 minutes or more to return too normal.

Compared to a healthy greyhound where the recovery time may vary from 2 to 10 minutes.

Any greyhounds exhibiting these signs must have a thorough heart examination by your veterinarian. In some instances this may involve testing the greyhounds heart function with an electrocardiogram as soon as possible after a run or trail.

Functions of blood
The average Greyhound has about 3 litres of blood that circulates through the body about every 30 seconds, and represents about 10% of the total body weight.

The red cells in the blood carry oxygen from the lungs and transport it to all of the body tissues.

On the return to the heart, the red blood cells absorb carbon dioxide from all the tissues and transport it to the lungs where it is exhaled.

The blood also contains the white cells whose primary role is to protect the body from invasion by bacteria, viruses, and other foreign material.

The blood aids in controlling body temperature by transferring heat from the internal areas of the body to the skin surface and lungs where it is dissipated.

Blood is also the vehicle for the distribution of hormones in the body that have a host of functions such as: maintenance of fluid balance, control of sexual activity, implementing the response to stress, thyroid hormone interaction with the metabolic functions of all the body cells, and a host of other hormonal reactions.

The body can survive the loss of many components, but it cannot survive without blood.
If 50% of the blood is lost the Greyhound will die within minutes even the rapid loss of as little as one litre can often be fatal without a prompt blood transfusion or fluid replacement.

Composition of the Blood
If you take a blood sample, place it in a tube with an anti clotting agent, allow it to stand for a couple of hours the blood would settle out into two major components.

On the bottom of the tube would be the heaviest components of the blood, the red and white cells and platelets. On the top section of the tube would be a slightly pale clear fluid, the blood plasma.

In the plasma are thousands of substances of varying size including all the hormones, antibodies, buffers, nutrients, enzymes, proteins, waste products and electrolytes as well as the major constituent water.

Many of these components of the blood can be measured and so provide valuable information about the health and physical status of the Greyhound.

Blood Components & Blood Tests
Before we look at specific Blood Tests, it is worthwhile looking at some of the major blood components, their specific function, and what it means if they are at either high or low levels in the blood.

Red blood Cells
HAEMOGLOBIN
This is the oxygen-carrying component of the red blood cells.

Any reduction in functional HAEMOGLOBIN will immediately affect performance.

The ability of HAEMOGLOBIN to carry oxygen to the tissues, may also be affected by the production of non-functioning HAEMOGLOBIN taking the place of normal HAEMOGLOBIN in the red blood cells, these are METHEMOGLOBIN and SULFHEMOGLOBIN.
This alteration to the HAEMOGLOBIN may be caused by treatment with anti-biotic SULPHONAMIDES such as SULPHANILAMIDE, SULPHATHIAZOLE and SULPHAPYRINE, or the feeding of raw onions in the diet, due to a component of onion oil called ALYLPROPYL DISULFIDE.

It is of some concern that many racing greyhounds are fed meat obtained from diseased or dead cattle that may have been treated with SULPHONAMIDES, or some similar substance and thereby impregnating the meat with a sufficient quantity of drug to cause non-functioning HAEMOGLOBIN to be formed.

Of greater concern is the fact that most of this meat is treated with a preservative.
The product used is either SODIUM SULPHITE or SODIUM METABISULPHITE; both destroy the THIAMINE (Vit. B1) in the diet.

In the long term this may cause severe nervous system damage and possibly even death.
SODIUM METABISULPHITE, under the right conditions, will breakdown to SULPHUR DIOXIDE.

This is a gas that at 500 parts per million will kill, and it is my opinion that there is a real good chance that both these products may cause problems with the HAEMOGLOBIN in susceptible Greyhounds.

Normal blood should contain 19 to 21 g/dl of HAEMOGLOBIN. As little as 0.5 g/dl of SULFHEMOGLOBIN or 1.5 g/dl of METHEMOGLOBIN is sufficient to cause rapid oxygen depletion of the body during exercise.

It is reasonable to assume that when a greyhound races over its normal distance while suffering this syndrome, all other aspects of the blood profile would show symptoms relating to severe stress.

Further investigation of the HAEMOGLOBIN may be of some value in greyhounds suffering sudden loss of stamina.

White Blood Cells
A decrease in total white blood cell count is generally associated with severe destruction, an excessive demand, or decreased production by bone marrow and lymphoid cells.

Greyhounds with a chronic low white blood cell count are immune deficient, and often develop secondary bacterial infections.

Low white blood cell counts may also be caused by toxin producing infections.

Bactericidal antibiotics, rather than bacteriostatic antibiotics should be used when there is an infection present, as well as a low white blood cell count.

Chronic inflammation or infection may cause an increase in the white blood cell count.

However, white cell numbers may also increase significantly without the stimulation of inflammation or infection, it may also be due to EPINEPHRINE release from excitement, and is often seen in easily excitable greyhounds and those suffering from the pre-race stress syndrome.

Neutrophils
Because neutrophils comprise a majority of the white blood cells, low neutrophil blood level is usually associated with a general decrease in all white blood cells.

Low neutrophil level (neutropenia) may be caused by increased use, or decreased production.

While severe inflammation, overwhelming bacterial infection or acute viral infection generally causes increased use.

Decreased production is often associated with immune deficiency due to depressed bone marrow and lymphoid cell production.
However inappropriate drug administration, as well as some Virus infections such as Canine Parvovirus may also cause a low neutrophil level.

Increased neutrophil level (neutrophilia) is usually caused by bacterial infections, but neutrophilia alone does not necessarily confirm the existence of an infection.

This is because other non-infectious problems, such as acute pancreatitis, severe stress, GLUCOCORTICOID therapy, or an increased workload and increased muscular activity may increase neutrophil levels.

Defects in neutrophil function may also increase neutrophil counts, because the existing neutrophils are not effective and more are produced in response to body requirements.

Lymphocytes
Decreased lymphocyte count (lymphopenia) may be caused by chronic infections, severe stress (HYPERADRENOCORTICISM), kidney failure or prolonged use of GLUCOCORTICOID injections.

As a general rule, low lymphocyte count indicates a viral infection, while prolonged lymphopenia could indicate that the body is unable to respond to the disease.

However, of the total number of body lymphocytes only 10% are in circulation, therefore it is not always possible to be certain in the short term, that low lymphocyte count (lymphopenia) indicates a poor immune response.

Increased lymphocyte count (lymphocytosis) is a common feature of chronic inflammatory disease, and could indicate a severe problem such as leukaemia or cancer.

Monocytes
Increases in monocyte count (monocytosis) may be seen in greyhounds suffering severe stress, chronic infection of the stomach such as a Protozoa infection or an abscess.

Monocyte numbers also increase in cases of neutrophil defects when monocytes are required to take over some neutrophil functions.

Eosinophils
Increase in eosinophils is usually the result of severe skin infection, chronic fungal infection or severe flea, roundworm, hookworm or heartworm infestation. However, similar symptoms may also be caused by an allergic reaction to wheat in the diet.

Circulating eosinophil level will rapidly decrease after an injection of cortisone or ACTH.

Basophils – Platelets
Any infection or infestation that results in an increase in eosinophils will generally also result in an increase in circulating basophils in addition, any increase in LIPID in blood will also cause an increase in basophils.

Platelets are produced by the bone marrow and any process that interferes with marrow production will reduce platelet levels, while increased platelet destruction as a result of the body's immune response to infection, also reduces platelet count.

Because the spleen is the main platelet storage site, increased platelet count may occur due to spleen contraction in response to excitement, chronic iron deficiencies, bone fractures or muscle trauma.

Anaemia
This is lower than normal levels of red blood cells, and may result from a decreased production, an increased loss, or an increased destruction of red blood cells.

Decreased production may occur due to loss of function of the blood forming tissue, as with some types of cancers or chronic infections.

Anaemia may also be caused by a lack of iron, B12, and or protein in the diet.

Increased loss may be due to a severe worm infestation or internal haemorrhage and blood loss via the intestines or urine.

While increased destruction is generally caused by a combination of several factors, such as infections, excessive workload or stress, increased levels of waste products in the blood, and may even be due to regular exposure to CARBON MONOXIDE from car exhaust fumes entering dog trailers, simply because CARBON MONOXIDE combines with HAEMOGLOBIN more readily than OXYGEN with HAEMOGLOBIN.

Packed Cell volume
When you ask for a basic blood test, some veterinarians will take a small blood sample, place it in what is called a hematocrit tube, and spin it in a centrifuge. In reality this will only provide a reading of the packed cell volume, and unless the current hydration status of the greyhound is taken into consideration, may even give a misleading result.

Blood Hematocrit Values in greyhounds are much higher than either humans or other breeds of dogs. The ideal balance between the solids in the blood and the blood plasma for a healthy racing greyhound is 60% solids and 40% plasma while values between 56 to 53% is considered borderline anaemia with anything below 53% anaemia that requires investigation and treatment.

Testing for Anaemia
MCV = Mean Corpuscular Volume MCH = Mean Corpuscular Haemoglobin
MCHC =Mean corpuscular Haemoglobin Concentration.

The results of tests for MCV, MCH and MCHC are generally used to determine the type and severity of the anaemia.

Blood tests fall into three basic categories:

1. Blood scan. A five-minute test that checks for any major changes from normal. It measures packed cell volume (PCV), total protein content (TP), and gives an estimate of white blood cell count (WBC), and haemoglobin content.

This test may not be available at many veterinary clinics, as it requires some specific machinery.

2. Full blood count. Takes about 30 minutes and gives a more detailed picture of the red and white blood cell numbers and distribution. This entails a direct count of the main types of white blood cells and helps identify infection, stress, allergy, and aid in evaluation of body defences against infections.

However, when you ask for a full blood count, many veterinarians will assume you require a blood profile and take blood to send to a pathology laboratory.

3. Blood profile. Often takes 24 hours, as it requires analysis by a pathology laboratory.

This is the most detailed of the available tests as it provides the red blood cell numbers and size, white blood cell numbers with individual type counts, the enzymes in the plasma relating to internal organ function and damage, the electrolytes indicating dehydration, kidney and liver function, calcium and phosphorus levels and a selected range of other body function tests.

This probably the most useful blood test, as it provides a total look at the Greyhounds state of health.

There is a reference range given for each substance in the blood that may be tested for, and when the substance tested for falls outside that given range, further investigations are instigated or treatments advised.

There is a very wide variation between the “normal low” levels of some blood components compared to the “normal high” level, that there is a broad range that is considered within acceptable limits.
Because these limits have been established as to what is "normal" for a broad range of greyhounds, ranging from young pups to older greyhounds, and therefore some values may not apply specifically to a highly trained athlete such as a racing greyhound.

This can make it difficult in some instances to determine the exact cause of some performance problems.

Personally I would be much happier if, instead of giving a broad range for each item, the ideal level for each substance was available.

That way any slight variations away from the ideal would give both the trainer and the veterinarian something to aim for, and would provide a much clearer picture of any problems large or small.

Unfortunately this is simply impossible to achieve due to the broad variation of many blood components within the normal range of even healthy racing greyhounds.

However, the way around this would be to have a blood profile performed on your greyhound at a time when you were absolutely satisfied that the dog was in a premium state of health and performing to the best of its ability.

This profile would then provide you with the ideal levels of each blood profile parameter for that specific greyhound.

Other Blood Components
Bilirubin
Bilirubin is one of the major body waste products that require excretion.
70% is derived from the destruction of cells mainly in the spleen and liver, 10% is from bone marrow, the remainder is from myoglobin breakdown.

Newly formed bilirubin is insoluble in water, and binds to circulating ALBUMIN.
This binding allows transport of bilirubin via the blood to the liver, and the now large BILIRUBIN/ALBUMIN complex prevents diffusion across cell membranes, and helps to confine bilirubin to the blood vessels.

Binding ability may be reduced by the drugs, SULPHONAMIDE and SALICYLATE or in animals suffering ACIDOSIS.

Bilirubin separates from albumin prior to entry into the liver cell.

Once inside, specific proteins bind the BILIRUBIN; it is then combined with GLUCORONIC ACID to form BILIRUBIN MONOGLUCORONIDE.

The importance of this process is that the bilirubin, previously insoluble in water, has now been transformed into a water-soluble compound, which is essential for it's excretion.

Even in the event of considerable liver damage this part of the system appears to continue to function efficiently.

Normally the now water-soluble bilirubin is excreted from the liver cells into the bile ducts.

However, this excretory system is extremely sensitive to various types of liver damage, and when the liver is under stress, increasing amounts of bilirubin are returned to the PLASMA.

On the other hand, in greyhounds with liver damage the TOTAL PLASMA BILIRUBIN may not increase significantly.

This is because dogs as a species, easily pass water-soluble bilirubin through the kidneys into the urine, and it is only when both liver and kidney damage occurs, that the plasma levels of bilirubin increase sharply.

The use of tests to measure the quantity of bilirubin in plasma is therefore not an accurate assessment of liver function in dogs.

As liver function is directly involved with bile production, measurement of SERUM BILE ACIDS is a more reliable procedure to test CURRENT liver function.

However, when total plasma bilirubin exceeds 1.0 mg/dl, one can observe a yellow colour of plasma in a spun micro hematocrit tube.

Impaired liver function leads to a decreased bile flow and is characterized by increased SERUM BILE ACID and ALKALINE PHOSPHATES (SAP) levels.

There are drugs that may also cause decreased bile flow, and increased serum bile acids; they include CORTICOSTEROIDS and long-term treatment with anti convulsants such as DILANTIN or PHENOBARBITAL.

Other drugs that may cause liver damage in dogs include MEBENDAZOLE (TELMINTIC) and possibly others such as OXIBENDAZOLE.

Liver damage may also be caused by AFLATOXIN, a mould found on grain type foods.
Protein, excess may indicate kidney disease.

Albumin
Albumin is synthesized in the liver from dietary amino acids.

Small amounts of albumin are lost in the urine and faeces, but most albumins are used in various metabolic processes such as tissue healing and repair.

The primary function of BLOOD SERUM ALBUMIN is to maintain the correct pressure of plasma and act as a carrier for various compounds such as bilirubin, calcium, drugs, hormones, toxins and others.

LOW BLOOD SERUM ALBUMIN (HYPOALBUMINEMIA)
Hypoalbuminemia may be caused by a large variety of clinical disorders; therefore the physical examination findings are variable.

Symptoms are generally related to the various metabolic processes involving albumin, such as poor tissue repair, soggy muscle tone, and in severe cases, signs of oedema when contributing factors are present, such as blood vessel damage or increased SERUM SODIUM with water retention.

When assessing the causes of the low serum albumin level, it is helpful to also consider the SERUM GLOBULIN level, because serum globulin is usually determined by measuring the total SERUM PROTEIN level, and subtracting the albumin concentration.

Globulin levels may provide some clues as to the causes of the low albumin level.
Even though, albumin and globulin levels should be interpreted independently, the ALBUMIN/GLOBULIN ratio may provide a useful indicator of liver function.

INCREASED BLOOD SERUM ALBUMIN (HYPERALBUMINEMIA)
The only recognized cause of hyperalbuminemia is dehydration, and should be corrected with appropriate fluid therapy.

Globulin
Most globulin (gamma globulin) is synthesized in plasma cells and lymphocytes as a part of the IMMUNOGLOBULINS.

The major function of this globulin is to act as antibodies in the immune response and to bind certain compounds in the body, such as hormones, and aid in their transport through the blood stream to their sites of action.

Approximately 3% of globulin is manufactured in the liver, these globulin are METAL BINDING GLOBULIN, and function to transport iron in the plasma.

When the diet is lacking in iron, this globulin increases in number.

However in some types of anaemia, chronic infections, or liver disease, there is a reduction of the metal binding globulin and as result there is a reduction in the ability of the red blood cells to regenerate.

The manufacture of functional globulin largely depends on the quality of the dietary protein; the best protein to produce globulin is milk protein, then egg, and then beef muscle protein.

LOW GLOBULIN (HYPOGLOBULINEMIA)
Causes of decreased globulin are due to decreased globulin production or increased globulin loss.

Decreased production may be due to inadequate diet or decreased liver function. Increased globulin loss may occur with kidney damage, depressed immune system, or immune system overload by toxin producing bacterial infections.

Low globulin level will make the animal more susceptible to infections.

HIGH GLOBULIN (HYPERGLOBULINEMIA)
High globulin count generally results from dehydration or increased globulin production; however, increased production is usually the result of chronic inflammatory conditions, both infectious and non-infectious.

Long-term excessive exercise, with increasing muscle breakdown and inflammation, as well as some types of cancer may also increase globulin production.

There is no doubt, that both human and animal athletes are more susceptible to infections, both viral and bacterial.

This appears to come about because of hard exercise, increased muscle destruction and general inflammation, changing the structure of the globulin and reducing its ability to provide the antibodies required for fighting off infections.

There are a variety of disorders that may be associated with increased globulin levels, the cause should be determined and treated appropriately, and if dehydration is present intravenous fluid therapy may be necessary.

Sodium
It is sodium that is primarily responsible for the level of fluid in the body and the distribution of water between the inside (Intra cellular) and outside (Extra cellular) of the cells.

Problems associated with deficit and excess of sodium reflect this function, deficit-causing dehydration, while excess could cause problems as severe as brain damage.

Cell membranes are relatively impregnable to sodium, but are easily penetrable to water, and any sodium ions that do gain access to the cell interior are actively pushed back into the extra cellular fluid by pumps in the cell membrane.

This pumping action depends on POTASSIUM IONS, and as sodium is pushed out of the cells, potassium is pumped in. In this way, potassium maintains the intracellular pressure.

Since water easily flows between the intracellular and extra cellular fluid, concentrations of both these major fluids is always the same.

Normal regulation of body fluid volume also depends up on a balance between water loss and water intake.

If increased drinking is not compensated by increased urine loss, body water must increase, end result over hydration of the cells.

On the other hand, if increased drinking does not compensate urine loss, body water decreases with resulting cellular dehydration.

The stimulation to drink is generated in, what is called the primary thirst centre of the brain, and the basic stimulation for the primary thirst centre is intracellular dehydration.

Stimulation of the primary thirst centre may also be triggered by volume and pressure receptors located in some of the larger blood vessels.

A reduction of 8% in blood volume or pressure can induce thirst and stimulate the release of an anti diuretic hormone (ADH).
While a 2% change in the extra cellular fluid volume will also cause ADH release and cause the kidneys to re-absorb water and concentrate the urine.

In addition to water re-absorption, ADH also increases the re-absorption of UREA.

This is important, as UREA influences the ability of the kidneys to re-absorb water.

However, stimulation of the primary thirst centre is not the only mechanism that determines water intake in normal animals.

Food intake as well as exercise also trigger thirst, in anticipation of possible water needs, before any actual cellular deficiencies can occur.

Sodium balance is closely regulated and maintained within narrow limits regardless of large variations in the dietary intake of sodium.
Although sodium is excreted from both the gastrointestinal tract and the kidneys, it is the kidneys that primarily regulate sodium balance.

Several factors influence this function; this includes a mineralocorticoid called ALDOSTERONE secreted by the ADRENAL CORTEX, the volume of blood flow through the kidneys, and the availability of ADH and UREA.

In a normal healthy dog nearly 75% of the fluid that passes through the kidneys is re-absorbed.
Essential to this function are ALDOSTERONE, ADH, UREA, and SODIUM.
Anything that affects the available levels of these substances will affect the ability of the kidneys to function normally.

So called acid neutralizers, alkalising diuretics, some infections (viral and bacterial), toxic substances and kidney disease, all reduce the ability of the kidneys to re-absorb water.
Causing various levels of dehydration and loss of essential substances, such as potassium.

LOW SERUM SODIUM (HYPONATREMIA)
Low sodium level can be due to decreased intake or increased excretion of sodium.

Any decrease in the serum sodium concentration following sodium loss is initially corrected by a reduction of both thirst and ADH secretion, reducing fluid intake and increasing urine volume.

In this manner serum sodium concentration is maintained, but at the expense of body fluid volume, causing rapid dehydration.

With progressive sodium loss, extra cellular volume keeps on reducing, and at a critical point, (8% reduction in blood volume) blood vessel volume receptors stimulate extreme thirst and ADH production, causing a water gain and a rapid decrease in serum sodium concentration.

Hyponatremia is characterized by signs of dehydration, decreased skin pliability, weak pulse, and the increased production of urine with low specific gravity. (POLYURIA)

HIGH SERUM SODIUM (HYPERNATREMIA)
High serum sodium causes water to transfer out of the brain into the extra cellular fluid, resulting in severe weakness and coma.

Severe heatstroke, excessive sodium administration, and kidney failure may also cause high serum sodium.

This is life threatening, and requires immediate and appropriate therapy, which will depend on the degree of dehydration.

Potassium
Of the potassium in the body, almost 98% is located within the cells; the remaining 2% is in the extra cellular fluid.

This situation is opposite to that which exists for sodium.

Maintaining high levels within the cell (intracellular) and low potassium levels outside the cell (extra cellular) is critical.

This is accomplished with the sodium/potassium pumps located in the cell membrane.

Low potassium within the cell may cause abnormalities in many biologic processes; including the cell volume, acid-base balance, production of RNA and GLYCOGEN, and dramatically reduces the ability of the cells to support muscle contractions.

Potassium intake and excretion determine the total body potassium content.

Equally important is the distribution of potassium between extra cellular and intracellular fluid.

If potassium intake were not matched by excretion, high serum potassium would soon result.

Under normal circumstances salivary and gastrointestinal potassium losses are minor, therefore excretion of potassium by the kidneys is vital.

On the other hand, the fluid that is filtered by the kidneys contains much more potassium than is present in the extra cellular fluid.
Therefore re-absorption of potassium by the kidneys is also vital to normal potassium balance.

In health, and without the interference of well meaning trainers, the kidneys efficiently maintain potassium within a narrow range.

However, in contrast to the kidneys ability to completely re-absorb sodium, small amounts of potassium continue to be lost even when potassium levels are low.

It is therefore important that potassium levels are maintained by the appropriate diet.

INTERNAL POTASSIUM BALANCE
This refers to the distribution of potassium within the cell (intracellular) and the potassium in the extra cellular fluid.

When potassium intake temporarily exceeds the ability of the kidneys to excrete it, the cells then take up more potassium to prevent the accumulation of excess potassium in the extra cellular fluid.

However, when kidney and gastrointestinal losses exceed potassium intake, transfer of potassium from the cells into extra cellular fluid occurs, delaying the onset of low serum potassium level.

Factors known to affect the handling of potassium by the kidneys are:
(1) The amount of potassium in the diet
(2) The amount of sodium and fluid being re-absorbed by the kidneys.
(3) BICARBONATE accompanying sodium through the kidneys, (bicarbonate increases the excretion of potassium).
(4) ALDOSTERONE, this is a mineralocorticoid produced by the ADRENAL gland, not only in response to dehydration, but also in response to an increased extra cellular concentration of potassium.

Aldosterone stimulates sodium re-absorption and potassium excretion by the kidneys, and therefore increases the likelihood of a low body potassium level in dehydration.

With chronic diarrhoea, loss of large quantities of potassium in faeces can occur.

Finally with vomiting, even though potassium losses in gastric juice may be minor, it is the loss of gastric juice HYDROCHLORIC ACID and resulting dehydration, which may cause METABOLIC ALKALOSIS and trigger a loss of large amounts of potassium in the urine and cause low serum potassium.

HYPOKALEMIA (LOW SERUM POTASSIUM) can occur because of decreased potassium intake, redistribution of potassium from outside the cell (extra cellular fluid) to inside the cell (intra cellular fluid), because of loss of potassium from the body, and in METABOLIC and RESPIRATORY ALKALOSIS.

HYPERKALEMIA (HIGH SERUM POTASSIUM) can occur due to increased potassium intake, an inability of the kidneys to excrete potassium, and in METABOLIC and RESPIRATORY ACIDOSIS.

In metabolic acidosis accumulation of HYDROGEN IONS in the extra cellular fluid causes the transfer of hydrogen ions to the intracellular fluid, potassium ions then shift from intra cellular to extra cellular fluid.

ACIDOSIS also influences the kidneys to retain more potassium due to the lower availability of BICARBONATE.

In RESPIRATORY ACIDOSIS, it is HYDROCHLORIC and CARBONIC ACIDS that displace potassium ions from the cells.

POTASSIUM LEVELS
Since 98% of body potassium is located within the cell and not available for measurement, determining whether or not potassium deficit is present, is an indirect process.

Normal POTASSIUM SERUM levels in a greyhound with ACIDOSIS may still indicate low cellular POTASSIUM levels, while a low POTASSIUM level in a greyhound suffering ALKALOSIS may indicate a redistribution of POTASSIUM from extra cellular fluid to intracellular fluid.

Therefore any determination of potassium levels in a blood test, must take into consideration both the hydration state of the Greyhound and the possible existence of either acidosis or alkalosis.

Severe tissue trauma, such as torn muscles with obvious oedema, or severe bruising may cause significant cellular release of potassium.

Good kidney function generally prevents HYPERKALEMIA.

However, greyhounds that are already suffering from some stress and dehydration may become affected.

Both high (HYPER) and low potassium levels (HYPO) cause muscle weakness.

Life threatening HYPOKALEMIA is rare, and treatment consists of giving POTASSIUM CHLORIDE tablets. (SLOW K)

Severe HYPERKALEMIA is potentially fatal due to heart damage, and treatment should not be delayed.

Treatment is generally aimed at reducing the effect of potassium on the heart by giving CALCIUM and reducing extra cellular potassium with intravenous SODIUM BICARBONATE or lactated Ringer's solution.

CHLORIDE and BICARBONATE
The determination of serum chloride and bicarbonate levels is mainly concerned with establishing the Ph of the blood, and to determine the existence of either ACIDOSIS or ALKALOSIS.

METABOLIC ACIDOSIS
Any clinical condition in which HYDROGEN IONS accumulate in the blood plasma, because of an excessive production of acidic waste, as in LACTIC ACIDOSIS due to excessive exercise and or reduced kidney function.

The excessive amount of hydrogen ions in the blood may cause the transfer of hydrogen ions into the cell, to maintain balance potassium ions then shift out of the cell.

Acidosis also favours retention of potassium in the body fluid, due to the lower levels of bicarbonate entering the kidneys.

Therefore greyhounds with metabolic acidosis may have normal or slightly higher levels of serum potassium, however the cells (intra cellular fluid) may be low in potassium (INTRA CELLULAR ACIDOSIS).

METABOLIC ALKALOSIS
Any clinical condition, in which there is a deficiency of HYDROGEN IONS in blood plasma, this may be caused by excessive intake of alkalising medication or from loss of acids due to severe vomiting.

INTRACELLULAR ACIDOSIS
In greyhounds suffering from HYPERADRENOCORTICISM, potassium depletion may cause an increase in HYDROGEN IONS within the cell, this is then followed by the excretion of acid urine despite the fact that the blood plasma may be alkaline, and the greyhound may be suffering from METABOLIC ALKALOSIS.

The use of alkalising agents in response to a dipstick urine test (acid urine) will only aggravate the condition.

Correcting the low potassium level is essential for recovery.

RESPIRATORY ACIDOSIS
Any clinical condition where CARBON DIOXIDE production in the body tissue, exceeds the ability of the lungs to remove it.

Respiratory acidosis is not common, except in extremely severe lung infections or when lung function is depressed, either under anaesthetic or from inappropriate drug use.

RESPIRATORY ALKALOSIS
Any clinical condition where CARBON DIOXIDE removal by the lungs, exceeds its production by body tissue.

Respiratory alkalosis is relatively common in low-grade lung inflammation, such as kennel cough, or any condition that includes hyperventilation.

Greyhounds suffering pre-race stress syndrome may suffer from respiratory alkalosis as a result of excessive barking.

However, body defence mechanisms in the case of respiratory alkalosis are extremely efficient and the condition normally clears quickly without treatment.

Unless of course, the greyhound stresses as a result of a hard race, and quite often greyhounds that suffer pre-race stress syndrome also suffer from Hyperadrenocorticism in which case the RESPIRATORY ALKALOSIS may be complicated by METABOLIC ALKALOSIS.

BODY FLUID Ph is normally maintained within narrow limits despite the continuous addition of large quantities of metabolic acids from the various processes within the body, and additions of carbon dioxide from cell function.

Three different types of mechanisms defend against any large changes of the blood Ph.

CHEMICAL BUFFERS, these include proteins, phosphates, sodium bicarbonate and haemoglobin.
Buffers are compounds that can absorb or donate HYDROGEN IONS as may be required.

SHIFTS IN IONS, HYDROGEN IONS may shift into (where they are chemically buffered) or out of the body cells as may be required.

RESPONSE BY BODY ORGANS, the kidneys can either retain or excrete acids, while the lungs, via increased or lowered breathing, can regulate ACID-BASE BALANCE by either retaining or expelling CARBON DIOXIDE.

Urea (BUN) Blood Urea Nitrogen
Urea is produced in the liver from AMMONIA and AMINO ACIDS in the blood.

After entering the circulation from the liver urea is filtered through the kidneys, where it plays an important part in the fluid re-absorption ability of the kidneys, and is then excreted in the urine.

LOW BLOOD UREA NITROGEN
Low BUN can occur because of decreased production or increased excretion.

Decreased production is most commonly associated with chronic liver damage or long term consumption of a diet severely restricted in protein.

Kidney disease, diabetes insipidus and some types of nephritis may cause increased excretion. However, increased excretion causing a low BUN is often seen in greyhounds with significant POLYURIA.

POLYURIA is the increased production of urine, generally urine of low specific gravity.

In some cases this is bought on by POLYDIPSIA (increased thirst) triggered by severe intracellular dehydration.

This in turn may be caused by severe stress, due to a hard run by an unfit greyhound, or one suffering from a bacterial or viral infection.

However, some instances of POLYURIA are in fact inflicted by the overuse of diuretic alkalising agents, the indiscriminate use of anti-inflammatory injections in injury treatments, or the use of GLUCOCORTICOID injections, in the belief, that they may improve the greyhound’s performance.

It must be said however, because greyhounds are generally on a high protein diet, normal or slightly lower BUN levels, may not give a true indication of the severity of problems relating to possible kidney disease, resulting in the POLYURIA / POLYDIPSIA syndrome, and a varying degree of dehydration.

INCREASED BLOOD UREA NITROGEN
An increased BUN may occur due to increased urea production by the liver, the intestinal tract, an excessively high protein diet, or a combination of any three.

However, decreased excretion of urea by the kidneys, is the most common cause of an increased BUN, and may be due to partial kidney failure, urinary tract obstruction, and or urinary tract infection.

It is generally believed that urea is relatively non-toxic, but other wastes that accompany increased BUN may cause toxicity and dehydration.

The method most used to treat the symptoms of an increased BUN is intravenous fluid therapy.

However a urine specimen obtained prior to treatment, should be submitted for a complete urine analysis, including sediment examination.

Specific treatment of the underlying cause should be started as soon as possible.

Creatine
Kidneys, liver, pancreas and amino acids are all involved in the synthesis of creatine.

Muscle contraction requires high energy, this energy is supplied by ATP (ADENOSINE TRIPHOSPHATE), this in turn, is produced by the action of CREATINE + PHOSPHATE using a specific enzyme as a catalyst.

Thus creatine acts as part of the high-energy reserve, which is required for rapid and sustained muscle contraction.

Injections of PHOSPHATE (COFORTA) will increase production of ATP, while injections of ADENOSINE TRIPHOSPHATE (DYNACLEINE) will directly increase high-energy reserves.
CREATINE + PHOSPHATE = ATP

How does it work?
Creatine (Cr) is one of the basic muscle energy stores in the body, particularly in fast twitch fibre.
It combines with phosphate to form PCr

During exercise the phosphate and creatine complex (PCr) is thought to be an immediate source for the high-energy phosphate groups with which to replenish ATP.

However there is some evidence to suggest that creatine only contributes significantly to ATP for the first few seconds of intense activity.

Creatine balance
In the racing Greyhound it is estimated that creatine has a turnover rate of approximately 3g per day, meaning that about 3 grams of creatine is irreversibly broken down to the waste product creatinine, and 3 grams synthesized to replace that.

There appears to be a natural balance between creatine within the cell and creatine circulating in the blood.

This balance can be altered only slightly by creatine supplementation in the diet.

Within a few days, intracellular Cr levels reach a new equilibrium, however a much smaller fraction of this additional creatine appears to be stored in the high-energy PCr form.

Finally the body appears to have a maximum level for circulating creatine, and supplementation reduces creatine production by the body.

SUPPLEMENTATION
Creatine can be found in many forms, raw muscle meat contains approximately 0.5% creatine by weight, commercial supplements are also available.

It has been suggested that Greyhound muscle have a maximum capacity of roughly 300-mmol creatine per Kg of muscle, making supplementation in excess of 30g per day pointless.

ENERGY EFFECT
A number of studies have examined the effect of creatine supplementation on performance.
The consensus appears to be that, while not increasing strength, creatine supplementation can increase the amount of energy available by about 8% and therefore increase the duration of function of fast twitch muscle fibers.

The mechanism of this enhancement is not yet clearly documented, but is most likely due to the increased availability of PCr.

Resting muscle does not require high energy, 60% of the energy required for maintenance of resting muscle is derived from direct use of carbohydrate diffusing into tissue from the blood circulation.

INCREASED SERUM CREATINE may indicate hyperactive thyroid, muscle disease or damage, infections or reduced carbohydrate metabolism.

INCREASED SERUM CREATININE
Creatinine, the waste product of creatine metabolism is excreted in the urine, and is not believed to be toxic, but is accompanied by toxic waste products that cause problems when there is a decreased excretion of Creatinine by the kidneys.

Complete urine analysis (not just a general dipstick test) is essential to finding the exact cause and determining the appropriate treatment.

Calcium
In addition to calcium's structural role in bone, the concentration of CALCIUM IONS within the body is critical for normal muscle contraction.

Muscle fibres are connected to the nervous system via neuromuscular junctions; these junctions release a substance called ACETYLCHOLINE, the released acetylcholine binds to special receptors on the muscle fibres.

This produces electrical activity by stimulating the movement of SODIUM and POTASSIUM IONS through the cell membrane, although this binding occurs for only a few milliseconds, it creates far more electrical activity than is required to stimulate muscle contraction.

This electrical activity generated on the surface of the muscle fibre is conducted into the cell, where it causes the release of CALCIUM IONS.
The calcium ions then modulate the acetylcholine and stimulate contraction of the muscle fibres. (MYOFIBRILS)

A pump within the muscle cell returns the calcium ions to the cell, keeping the concentration of calcium ions in the myofibrils at an extremely low level, except when required for the next muscle contraction.

Calcium is present in the extra cellular fluid in three forms, IONISED, bound to ALBUMIN, or combined with CHLORIDE or BICARBONATE.

ONLY IONISED CALCIUM IS BIOLOGICALLY ACTIVE IN MUSCLE CONTRACTION.

Most laboratory methods for measuring SERUM CALCIUM simply measure the total serum calcium, however this provides no real guide to the availability of IONISED CALCIUM.

Nor does simply measuring total serum calcium take into consideration changes in calcium value's depending on blood Ph.

ALKALOSIS decreases ionised calcium, while ACIDOSIS has the opposite effect.
Special equipment is needed to measure ionised calcium.

LOW SERUM CALCIUM (HYPOCALCEMIA)
The initial symptom of low serum calcium may simply be an episodic weakness after a hard run.

If severe, the symptoms may include muscle tremors, panting, nervousness, seizures, and increased body temperature.
These signs may be sporadic instead of constant.

HYPOCALCEMIA is potentially life threatening and should be treated without delay.

HIGH SERUM CALCIUM (HYPERCALCEMIA)
Although high serum calcium in greyhounds is rare, depending on the cause, the symptoms may include; depression, anorexia, constipation, weakness, polydipsia / polyuria (excessive water drinking and urine production) and cardiac arrhythmia's.

When high serum calcium is coupled with elevated SERUM PHOSPHORUS levels it may cause soft tissue mineralization and severe kidney damage due to kidney calcification.

Severe HYPERCALCEMIA may be fatal.

Phosphorous
Essential for normal bone strength and Phosphates are required in conjunction with Creatine for the formation of the energy component used in muscle contraction

ALT (ALANINE TRANSAMINASE)
INCREASED ALT
Increased levels of this enzyme are due to either increased cellular release or increased cellular production.

ALT is located in the liver cells (HEPATOCYTE’S) and is released whenever there is liver cell damage or destruction.

ALT is liver specific in dogs; other enzymes released during liver damage include AST (ASPARTATE TRANSAMINASE) and LDH (LACTATE DEHYDROGENASE).

However AST is normally present in higher concentrations than ALT, except in liver disease when ALT exceeds AST.

The levels of increased SERUM ENZYME activity equals the number of liver cells currently being damaged, but provides no information regarding the ability of the liver to heal, nor the current ability of the liver to function.

Neither ALT nor SAP (SERUM ALKALINE PHOSPHATASE) determinations are liver FUNCTION tests.

It is also important to note that, because the half-life of serum enzymes released during liver damage is only 2-4 day's, liver failure may still exist with NORMAL ENZYME levels.

DECREASED ALT there is no known significance to decreased serum ALT.

AST (ASPARTATE TRANSAMINASE)
Increase may indicate heart damage, jaundice, acute hepatitis, or severe tissue damage.

ALP (ALKALINE PHOSPHATASE) (ALK PHOS)
Unlike ALT there are certain enzymes that can gain access to the blood circulation without damage to the cells that produce these enzymes.

Significant increases in ALP are usually caused by increased cell production, and not usually by cell destruction.

Tissues and cells known to produce this enzyme include cells in bone, liver, bile duct, intestine and placenta.

Increased ALP levels are also seen in greyhounds injected with CORTISONE and those suffering severe stress accompanied by HYPERADRENOCORTICISM.

Although the precise mechanisms are unknown, it has been reported that GLUCO-CORTICOIDS also cause increased production of ALP (ALKALINE PHOSPHATASE).

The duration of GLUCOCORTICOID induced increase in ALP is unpredictable, but it can take several months for the ALP levels to normalize.

When the blood profile shows increased levels of both ALP and ALT, check for and rule out, Hyperadrenocorticism, liver disorders, chronic active hepatitis, liver infection, or acute pancreatitis.

CPK (CREATINE PHOSPHOKINASE)
Increase may indicate muscle damage or recent run.

GGT (GAMMA GLUTAMYL TRANSPEPTIDASE)
Increased in liver or biliary disease, hepatitis or pancreatitis.

GMT (GLUTAMYL TRANSFERASE)
Increase may indicate hepatitis or pancreatitis.

GOT (GLUTAMIC OXALOACETIC TRANSAMINASE)
Increase may indicate heart muscle damage.

GPT (GLUTAMIC PYRUVIC TRANSAMINASE)
Increase may indicate liver damage.

IDH (ISOCITRIC DEHYDROGENASE)
Increase may indicate liver damage, brain tumour or meningitis.

LDH (LACTIC DEHYDROGENASE)
Increase may indicate recent heart damage, levels return to normal after 5 days.

Glucose
Glucose levels are a result of glucose production and use in the body.

Sources of blood glucose are EXOGENOUS (food intake) and ENDOGENOUS (produced within the body).
When food is not available, continuing body requirements causes ENDOGENOUS glucose production.

The liver, under hormonal influences, maintains blood glucose for about 24 hours.

Thereafter, body proteins (mainly muscle) are used as the main source of ENDOGENOUS glucose, resulting in a reduction of muscle bulk.

Several hormones increase blood glucose; these include GLUCAGON, GLUCOCORTICOID, EPINEPHRINE, GROWTH HORMONE and PROGESTERONE.

The PANCREAS, using GLUCAGON and INSULIN controls the normal regulation of blood glucose levels.

When blood glucose decreases, GLUCAGON output from ALPHA cells in the PANCREAS increases and INSULIN secretion from PANCREATIC BETA cells is suppressed.

LOW BLOOD GLUCOSE (HYPOGLYCAEMIA)
In the racing greyhound, HYPOGLYCAEMIA is seldom seen in isolation, but generally as part of a syndrome that may include signs of liver failure, ADRENOCORTIAL insufficiency and acute PANCREATITIS.

The severity of the symptoms of HYPOGLYCAEMIA is related more to the speed of the decline in blood glucose, than a gradual decrease.
It generally cause few signs other than, intermittent weakness after exercise or occasionally 2 to 6 hours after eating.

With persistent HYPOGLYCAEMIA check for PANCREATIC tumours.

HIGH BLOOD GLUCOSE (HYPERGLYCAEMIA)
The most common cause of mild to moderate HYPERGLYCAEMIA is stress or excitement. Stress causes GLUCOCORTICOID secretion by the adrenal gland, which results in the liver producing more GLUCOSE.

While excitement causes CATECHOLAMINE release, which also results in the liver producing glucose.

In severely stressed greyhounds suffering from HYPERADRENOCORTICISM other signs may include, POLYDIPSIA (increased thirst), POLYURIA (excessive amounts of urine), thin skin, some hair loss (due to THYROID suppression) and possibly abdominal distension.

It is not usually necessary to treat the symptoms of HYPERGLYCAEMIA, except to change and treat the underlying causes of the stress.

Cholesterol
Fatty acids are an essential part of the diet, and influence the growth of skin, healthy hair, kidney function and optimum utilization of energy.

The ability to breakdown the fatty acid to components that can be absorbed into the bloodstream depends upon the availability of bile and pancreatic juice.

The CHOLESTEROL part of the fatty acids is also required for maintaining energy levels, and the production of steroid hormones.

Cholesterol from egg yolk, meat and cod liver oil is easiest to absorb, while the addition of fatty acids from plant oils to the diet, such as peanut, corn or safflower oil reduces the absorption of cholesterol.

The body also synthesizes cholesterol, mainly in the liver.

The cholesterol in the bloodstream is mostly derived from cholesterol synthesized by the body, while the fatty acids in the diet contribute to fat stores.

Approximately 50% of all body fat are stored in subcutaneous tissue, while less than 5% is stored in muscle tissue.

The liver plays a central role in the processing of cholesterol, both by synthesizing cholesterol and adding it to the blood, and removing it by oxidization and excreting it into the bile.

However, both the thyroid and the adrenal gland influence the speed at which the liver processes fatty acids and cholesterol.

Low thyroid levels may lead to increased fat storage, as well as elevated levels of cholesterol in the blood, while prolonged high levels of blood cholesterol may further reduce thyroid function.

Hyperadrenocorticism (severe stress) will also reduce thyroid function and increase the levels of cholesterol.

THYROID GLAND and THYROXINE
The principal function of THYROID HORMONE (THYROXINE) is to control and stimulate the rate of metabolism of the body.

When levels of THYROXINE are decreased it results in decreased physical and mental vigour.

There are a number of factors that influence the function of the thyroid.

IODINE METABOLISM
Iodine is essential to the production of Thyroxine and is the only known function of iodine in the body.

THYROID STIMULATING HORMONE (TSH)
A hormone produced by the pituitary gland stimulates activity of the thyroid gland by increasing the uptake of iodide, and stimulating its conversion into Thyroxine.

THYROID BINDING GLOBULIN (TBG)
Serum proteins that act as carrier agents for Thyroxine and distribute it throughout the body
Anything that affects the IODIDE metabolism, the production of TSH, or the binding of Thyroxine to GLOBULIN, affects the function of Thyroxine in the body.

HYPERADRENOCORTICISM (STRESS) causes a rapid decrease in TSH, (thyroid stimulating hormone) greyhounds suffering this condition are often HYPOTHYROID. (Low serum Thyroxine).

ANABOLIC STEROIDS decrease the levels of available TBG (Thyroxine binding globulin) and so reduce the level of Thyroxine in the body.

There is also a genetic factor involved in thyroid function, in animals where it exists; much of the body iodide is not available for Thyroxine production.

LOW PLASMA THYROXINE, as demonstrated by a test to determine the globulin bound level of Thyroxine (T4) or a test to determine the level of Thyroxine not bound to globulin (free T4), is extremely common in the racing greyhound, in many cases this may be due to severe stress.

Generally treatment consists of providing oral supplements of THYROXINE SODIUM.
The initial dose should be small, and increases made at 14-day intervals until the desired metabolic balance is achieved.

At this time it may also be worthwhile to provide the dog with extra iodine in the diet, by adding a pinch of iodised salt to the main meal each day.

Iodine may also be given as a supplement: 2 drops of 2.5% Iodine in a cup of low fat milk, given as a drink every third day for 5 doses.

ADVERSE REACTIONS
Some dangers exist in providing excessive doses of oral Thyroxine in an attempt to rapidly increase thyroid hormone levels.

(1) Administration of Thyroxine further depresses TSH production, possibly compounding the original cause.
(2) Excess levels of Thyroxine may lead to heart muscle damage, and or bone fractures.
(3) A single dose may take up to a week to develop its maximum response, and repeated daily doses may have a cumulative effect, which does not become fully apparent for 14 day’s or more.

The initial dose should be small, usually 100 microgram daily, and increases made at fortnightly intervals by 50 microgram until the correct metabolic balance is achieved.

Overdose may cause restlessness, increased excitability and the possibility of heart muscle damage during strenuous exercise.

As well as supplementing the thyroid hormone levels with Thyroxine sodium, every effort should be made to rectify the training program and reduce the stress levels.

PARATHYROID HORMONE (PTH)
Small glands that are attached to the thyroid gland produce PTH.

PTH acts in conjunction with other hormones to control the CALCIUM and PHOSPHATE levels in the body.

When calcium intake is insufficient, it elevates the serum calcium level by dissolving CALCIUM SALTS in the bone and increasing the excretion of PHOSPHORUS.

The primary function of the PARATHYROID HORMONE is to maintain the concentration of IONISED CALCIUM in the plasma within a narrow range, in spite of wide variations in CALCIUM intake.