The Components of a Stethoscope. An Introduction to Canine Cardiac Auscultation. Classification of Arrhythmias. Normal and Altered Sinus Impulse Formation. Problems and Strategies for Murmur Localization. The Most Common Murmurs Afflicting Dogs.
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The Components of a Stethoscope
Most stethoscopes are designed with a bell and a diaphragm. The diaphragm is designed to pick up high frequency sounds and should be held firmly against the skin. The bell is designed to amplify lower frequency sounds when applied with light pressure. When using the bell, avoid applying firm pressure because the skin beneath the bell will act as a diaphragm and negate the amplification of low frequency sounds (Fox, 1988). The ear pieces should fit comfortably in your ear canals. If the stethoscope comes with different sized ear pieces, select the ear pieces that form the tightest seals in your ear canals. The tubing connecting the binaurals to the bell-diaphragm may be single or double layered. Double layered tubing eliminates more background noise.
How To Use a Stethoscope Correctly
For auscultation to be effective, it should be performed in a quiet room with little extraneous noise. The stethoscope is most effective if:
1. When placed in the ears, the binaurals follow the same direction as the ear canals (see diagram below).
2. The ear pieces fit snugly in the ears forming a tight seal and the hand holding the stethoscope is still, relaxed and placed against the animal with a constant amount of pressure.
An Introduction to Canine Cardiac Auscultation
The four basic principles required for successful auscultation are:
1. Correct use of the stethoscope.
2. Recognition of external landmarks that correspond to valve locations and that due to acoustical effects within the heart, the locations where sounds are heard loudest do not necessarily correspond to their anatomical source.
3. Correct differentiation, interpretation and understanding of normal versus abnormal sounds. Studies have shown that both students and veterinary practitioners can correctly describe the physical features of heart sounds, however, their ability to correctly interpret these sounds is often lacking (Naylor et al., In Press). This finding may be because traditional teaching methods rely on a verbal description of an audible anomaly rather than actual audio recordings. The authors of this website hope that with the multimedia technologies used herein, specifically the pairing of actual cardiac audio recordings with visual interpretation, individuals will improve their diagnostic and interpretive skills. For further information on cardiology, you may consult "Hearing Horse Hearts: An Interactive Guide to Equine Cardiac Auscultation" (Naylor, 2000).
4. The ability to convey your understanding and interpretation of what you heard to others using standard veterinary terminology.
The canine heart projects into both thoracic cavities, particularly the left, from the third to the sixth intercostal space. The long axis of the heart is rotated cranially so that it lies at an angle with the base more cranial than the apex. The base of the heart is fixed by the great veins and arteries while the apex can move freely within the pericardial sac. The so-called right and left sides of the heart are more correctly understood to be the dextro-cranial and levo-caudal sides because the left ventricle lies behind and slightly left of the right ventricle. The left ventricle is more conical and massive than the right ventricle which is more crescent shaped.
If the dog is standing square, much of the heart lies medial to the triceps mass. A horizontal line drawn through the point of the shoulder lies slightly above the level of the heart valves. As opposed to using features of the forelimbs (e.g. The point of the shoulder and position of the olecranon) to locate heart valves, palpation of the apex beat is more accurate because its position is independent of the dogs forelimbs.
Internal landmarks for the heart valves largely rely upon their positions relative to intercostal spaces and costochondral junctions. The following guidelines (Tilley and Goodwin, 2001) may be helpful for auscultation.
Cardiac auscultation should be performed in a quiet room free of excessive noise. Cardiac auscultation should also be performed as soon as the animal enters the exam room or when the dog is stressed since this increases the probability that a transient or subtle murmur will be detected. The probability of detecting a murmur increases with stress because sympathetic activation increases heart rate, cardiac contractility and cardiac output. Turbulent flow, which gives rise to murmurs, is more likely at higher blood velocities.
Cardiac auscultation should proceed in a logical manner. The apex beat (mitral valve area) should be palpated and the heart rate measured either by cardiac auscultation or palpation of the femoral pulse. The femoral pulses should be palpated in each hindlimb and compared for fullness, sharpness and regularity. Next the femoral pulse should be palpated simultaneously with cardiac auscultation in order to detect pulse deficits due to arrhythmias. Each valve should be ausculted in the order Mitral, Aortic, Pulmonic (acronym MAP). Some palpate the apex beat (mitral valve area) and move cranially from there. However, if you wish to auscult in a particular intercostal space it is easier if you start counting spaces from the last rib (13 th) cranially.
An arrhythmia or dysrhythmia is a deviation from the regular rhythm. In dogs this may be normal or abnormal and may result from abnormal cardiac impulse formation, conduction, rate or regularity.
Regularity refers to the predictability of an arrhythmia. Some arrhythmias occur in a predictable fashion and are said to be regularly irregular. These rhythms may be normal (e.g. sinus arrhythmia) or pathological. In others the onset of the next beat is completely unpredictable and the rhythm is said to be irregularly irregular (e.g. atrial fibrillation). Irregularly irregular rhythms are pathological in origin.
Classification of Arrhythmias
Tilley and Goodwin (2001) classify arrhythmias according to:
Supraventricular arrhythmias arise from the atria or AV node whereas ventricular arrhythmias arise from the ventricles.
Arrhythmias with slow rates are bradyarrhythmias while those with fast rates are tachyarrhythmias.
Fibrillation is a rapid, irregular, chaotic rhythm while tachycardia is a rapid but regular rhythm.
Normal Sinus Impulse Formation
Sinus arrhythmia is a regularly irregular sinus rhythm which is a normal finding in most dogs (especially brachycephalic breeds). Sinus arrhythmia is characterized by slight variations in the S1-S1 interval. These variations are related to changes in vagal tone to the heart and are often associated with inspiration (negative pressure created in the thorax) or use of sedative or anesthetic drugs. You can demonstrate sinus arrhythmia by palpating the radial artery on your wrist. Once you feel your pulse take a big deep breath and you should feel your pulse quicken and then slow down as you exhale.
Altered Sinus Impulse Formation
Sinus Bradycardia (Slow Heart Rate)
Sinus bradycardia has a regular rhythm and may result from systemic disease (renal failure), toxicities, increased vagal tone, elevated intracranial pressure or compression of the eyeball, hypothermia, hypothyroidism or drugs (tranquilizers, propranolol, morphine, various anesthetics) (Fox, 1988). Sinus bradycardia is diagnosed when the heart rate is less than 65 beats / minute and an ECG shows sinus rhythm.
Sinus Tachycardia (Fast Heart Rate)
Sinus tachycardia; often caused by stress; is the most common arrhythmia observed in dogs and has a regular rhythm. Sinus tachycardia may result if there is increased metabolism and oxygen demand or increased requirement for cardiac output (pain, fright, excitement), pathology (fever, shock, anemia, hypoxia, hyperthyroidism) or pharmacological agents (atropine, epinephrine, ketamine) (Fox, 1988). Sinus tachycardia is diagnosed when the heart rate is more than 160 beats / minute for most dogs (>180 bpm for small / toy breeds or >220 bpm in puppies) and an ECG shows sinus rhythm (Fox, 1988).
Altered Supraventricular Impulse Formation
Atrial fibrillation is a common pathological arrhythmia in dogs. Auscultable characteristics of atrial fibrillation include a completely unpredictable rhythm, sometimes called a "jungle-drums" rhythm. Listen for long diastolic pauses between some beats and very short intervals between others. Sometimes the beats are so close together that S2 is not generated and two S1 sounds follow each other. The other hallmark of atrial fibrillation is a pulse deficit. Sometimes this can be detected because there is a large disparity between the heart rate and the pulse rate. If the heart beat is slow it is more reliably detected by simultaneous auscultation and palpation of the pulse. Normally every S1 heart sound is followed by a pulse wave. Abscence of a wave is called a pulse deficit.
The most common causes of atrial fibrillation are chronic atrioventricular valvular insufficiency in small breeds, dilated cardiomyopathy in large breeds, and congenital heart defects. Less common causes include heartworm disease, cardiac trauma, digitalis toxicity and severe metabolic disorders (Fox, 1988). Auscultable or palpable characteristics of atrial fibrillation include inconsistently filled femoral pulses, detection of an S1 without an S2 and a pulse deficit.
Disrupted Impulse Conduction
Second Degree Atrioventricular (AV) Block
Second degree AV block may be of two types: Mobitz I, usually type A or Mobitz II, usually type B. The two types of second degree AV block are best distinguished by ECG. Mobitz I is a normal finding in dogs, especially in young animals and disappears with exercise. Mobitz II is pathological in origin and will not disappear with exercise. Both types of second degree AV block are manifested by a dropped beat detectable during auscultation. By exercising and immediately ausculting the dog, you can determine if the AV block is a Mobitz I (the dropped beats have disappeared) or Mobitz II (the dropped beats are still auscultable). Second degree AV blocks can be associated with sinus arrhythmia, increased vagal tone, supraventricular tachycardia, electrolyte imbalances or drugs (digitalis, intravenous atropine, xylazine) (Fox, 1988).
Murmurs are sounds produced by turbulent blood flow. Rapid flow, a wide vessel, low blood viscosity and an uneven or constricted vessel wall all predispose to cardiac murmurs. They can be physiological, for example high blood flow though the aortic outflow tract. Pathological murmurs reflect heart disease, for example degeneration and roughening of a valve surface. Veterinarians require a uniform method of describing murmurs to facilitate communication between each other via a common understanding. Five parameters have been developed that serve to describe all of the important aspects of a murmur. Of the five parameters, the most important ones are position in the cardiac cycle, intensity, duration and pattern of intensity. The point of maximal intensity (PMI) identifies the location where the murmur is heard loudest and is often described using the valve location nearest (e.g. Mitral valve area). On the following page is a table summarizing the parameters and their descriptions (Naylor, 2000). In dogs, systolic or continuous murmurs are more common than diastolic murmurs .
In describing the duration of murmurs, pan- refers to a murmur that obliterates both heart sounds either through systole or diastole. Holo- refers to a murmur that lasts throughout systole or diastole but does not obliterate any heart sounds. A continuous or machinery murmur lasts throughout most or all of systole and diastole and may or may not obliterate heart sounds. Early- and late- describe murmurs that are positioned closer to one heart sound than to another. Crescendo, decrescendo or diamond are terms that describe the intensity profiles of murmurs as increasing, decreasing or increasing and then decreasing in loudness. Musical and blowing are terms used to describe the frequency profile of a murmur. Grade refers to the absolute intensity of murmurs determined on a 6 point scale where the higher the grade the more severe the murmur (Example: Grade 2 versus a grade 5 regurgitant murmur).
Research shows that most clinicians correctly describe the grade of a murmur. Localization of the murmur to systole or diastole is less consistent. A clue is the timing of the heart sounds (systolic murmurs occur in the short pause), however loud murmurs can be perceived as being of longer duration than they really are (Naylor et al., In Press). Another useful method is to palpate the pulse during auscultation. Pan- or holo-systolic murmurs should be heard coincident with the pulse wave.
Problems and Strategies for Murmur Localization
On the left side, the pulmonic and aortic roots lie next to each other and it is difficult to separate their respective valvular sounds. Both produce sounds that are best heard cranio-dorsally on the left side of the thorax at the second or third intercostal spaces. Since the aortic valve is more centrally located and produces louder sounds some aortic murmurs are also heard on the right side. Mitral valve problems produce sounds that are heard more caudally centered on the fourth or fifth intercostal space. On the right side, tricuspid and ventricular septal defects produce murmurs that are heard ventrally around the fourth or fifth intercostal space. A problem with localizing the origin of murmurs is that loud murmurs can radiate over a wide area and on both sides of the thorax. Despite this, the point at which they are loudest is often close to the lesion.
Sometimes it may prove challenging to correctly identify the likely origin of a murmur. Generally by following a logical process like the one outlined here, insight may be gained into the type of murmur being dealt with. First of all the stethoscope should be moved around to all the valve areas on each side of the thorax in order to ascertain where the PMI is located and which; if any; valve is involved. With the location of the PMI known the murmur's intensity may be accurately graded and the character and quality judged. Finally, by simultaneously ausculting the PMI and palpating the femoral pulse an accurate indication of the position and duration of the murmur within the cardiac cycle may be obtained. Additionally, note that by examining the animal as soon as it enters the exam room or when it is stressed, the probability of detecting a transient or subtle murmur increases because the intensity increases in accordance with the sympathetic effects of stress.
The Most Common Murmurs Afflicting Dogs and their Features
In order of prevalence:
Mitral Reguritation; the result of mitral insufficiency; allows backflow of blood into the left atrium. Typical features of mitral regurgitation include a normal to increased arterial pulse, a PMI located at the left apex, a plateau or decrescendo quality and systolic position in the cardiac cycle (Fox, 1988). Mitral regurgitation is most often the result of acquired valvular disease (e.g. mitral valve endocardiosis) and is usually observed in older dogs.
Patent Ductus Arteriosus (PDA)
Patent ductus arteriosus results when the ductus arteriosus fails to close properly (functional closure normally occurs by 72 hours after birth while anatomic closure is complete within the first few weeks). PDA is therefore most commonly seen in young dogs with a higher prevalence in purebreds and females (Fox, 1988). This murmur will feature an increased arterial pulse, a normal to increased venous pulse, a PMI located at the left base and a machinery or continuous quality as it is present throughout most or all of systole and diastole (Fox, 1988).
Tricuspid regurgitation; the result of tricuspid insufficiency; allows backflow of blood into the right atrium. Like mitral regurgitation, tricuspid regurgitation is most often caused by acquired valvular disease and is usually observed in older animals. Features of a tricuspid regurgitant murmur include an increased venous pulse, a PMI located at the right apex, a plateau or decrescendo quality and a systolic position in the cardiac cycle (Fox, 1988).
The following two diagrams represent the locations where specific cardiac pathologies will be auscultated best.
The Apex Beat
The apex beat is an impact vibration produced at the start of ventricular contraction as the heart hits the chest wall. In the normal dog it is palpated on the left side, ventrally in about the fifth intercostal space. The apex beat should be identified by palpation before the heart is listened to. It is important in lesion localization because the mitral valve lies close by and S1 is loudest at this point.
Some of the common terms used in cardiology are:
Blowing describes the frequency profile of a murmur in which there is no single predominant frequency.
Continuous murmurs occur throughout both systole and diastole and are often associated with patent ductus arteriosus (PDA).
Crescendo describes an intensity pattern of a murmur that increases as it progresses towards completion.
Crescendo-Decrescendo - See Diamond-Shaped
Decrescendo describes an intensity pattern of a murmur that decreases as it progresses towards completion.
Diamond-Shaped refers to an intensity pattern of a murmur that first increases and then decreases towards completion.
Fibrillation refers to the situation in which muscle tissue spontaneously enters a state of rapid, irregular and completely random contractions.
Flutter describes a state of rapid, regular and uniform muscular pulsations or contractions in the range of 200-320 per minute.
Holo- describes the duration of murmurs which last from the end of S1 to the beginning of S2 or the end of S2 to the beginning of S1 and these murmurs do not obliterate S1 or S2.
Insufficiency refers to the situation in which a heart valve fails to close properly. Blood flows against its normal course producing turbulence and a murmur.
Machinery describes a murmur that occupies most of systole and diastole and may be used interchangeably with continuous.
Musical describes the frequency profile of a murmur when there is a single prominent primary or fundamental frequency with secondary harmonics.
Pan- describes the duration of murmurs which last from the beginning of S1 to the end of S2 or the beginning of S2 to the end of S1 and thus the murmur obliterates both of these heart sounds.
PDA (Patent Ductus Arteriosus)
PDA is a congenital condition characterized by the post-natal persistence of a lumen in the ductus arteriosus between the aorta and the pulmonary artery. PDA is often manifested by a continuous murmur.
Plateau describes an intensity pattern of a murmur that remains constant through to completion.
Stenosis describes the situation in which a heart valve fails to open properly or the chamber or vessel is abnormally narrow and the normal flow of blood is impeded.
Thrill is a vibration caused by turbulent fluid movement through an incompetent valve which is palpable on the thoracic wall. Thrill is typically observed with grade 5 or 6 murmurs.
Regurgitation results with valvular insufficiency and is characterized by blood flow against its normal course. In canines mitral valve regurgitation is the most common regurgitant-type murmur that will be encountered.
VSD (Ventricular Septal Defect)
VSD is a congenital condition characterized by the persistent patency of the ventricular septum post-natally thus allowing blood to flow directly between the ventricles. Since the blood can bypass the pulmonary circulation cyanosis may be present in addition to a grade 5/6 systolic murmur.
canine cardiology arrhythmias murmur dog
Normal Resting Heart Rate Values for Canines
The "normal" heart rate for canines varies with the age, physical size, breed, level of arousal and physical condition of the animal (Tilley and Goodwin, 2001). Smaller dogs have faster heart rates than larger ones. Compare the recordings from an adult Poodle, with that from a greyhound, and use your watch to practice taking the heart rate. As a general rule, clinicians will take the heart rate over a period of 10 or 15 seconds depending on how tachycardic the animal is. If you have difficulty counting the faster rate try counting in tens and remembering every set of ten by extending a finger.
PSYCHOPHYSIOLOGY OF STRESS ACCORDING TO HANS SELYE
General Adaptation Syndrome (GAS): Hans Selye is credited with creating the first definition of stress as a non-specific response of the body to any demand made upon it. Selye's theory about the effects of stress he demonstrated to be applicable to any sort of stress.
The 3 stages of the GAS are:
Alarm Reaction: Similar to fight or flight.
Resistance: Struggle to overcome, hard work, limited rest/sleep.
Exhaustion: Body systems crash, fatigue, errors, irritability, vulnerable to illness (colds, flu, acne).
Non-specific stress response: Selye's theory was that injury, overload and fear all produce the same body reaction. He believed that both eustress and distress both produced the same response in the body. Both situations, he said, resulted in some degree of wear and tear in the body which finally accumulated to produce aging.This theory was over-simplified as you will see below.
A review was published by Selye in 1946, where he already gives a comprehensive theory of the general adaptation syndrome which is supported by experimental facts. He also talks about the possibility that diseases of adaptation do exist. He states that, after exposure to stress, initially there is shock, which is followed by a counter shock phase, and this gradually goes into a stage of resistance. If, however, the stressor persists, resistance may go into exhaustion and death may ensue. He points out that specific and nonspecific resistance follow the same course but this latter "cross resistance" will fall much sooner and stays below normal during the period of resistance. He also presents data of blood sugar and chlorine changes and points out that white blood cell counts rise invariably during stress, regardless of the stressor used. The changes in the adrenal cortex and of thymus involution are also illustrated histologically. The adrenal cortex becomes wider with loss of lipid granules and the border between the zona fasciculata and reticularis is no longer distinct. The thymus shows a depletion of cortical thymocytes. Nuclear debris is evident and pyknotic thymocyte nuclei are abundant. He notes that this "accidental involution" becomes most pronounced during the countershock phase when the adrenal cortex reaches its maximum development. Large macrophages engulf the dead thymus cells and carry them away through the lymphatics. At the same time he noted that thymic reticulum reverts to its origianl epithelial type and the cells become roundish or polygonal and rich in cytoplasm. When involution is most acute the entire organ is distended with jelly-like edema. He points out that lymph nodes, the spleen and other lymphatic organs are almost as markedly affected as the thymus, although they do not involute quite as rapidly and their involution cannot be completely prevented by adrenalectomy.
Today we know that a variety of insults, including trauma and infection stimulate the release of chemotactic-, proinflammatory cytokines, and a whole host of other mediators from a variety of cells in the damaged area that include mast cells, endothelial cells, platelets. The released mediators attract blood borne leucocytes, such as neutrophilic granulocytes, monocytes/macrophages, lymphocytes, eosinophils and basophils that release additional mediators, and thus contribute to the inflammatory response. In some cases certain cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-a (TNF-alpha) and interleukin-6 (IL-6), become detectable in the blood and function as acute phase hormones. They act on the brain causing fever and other functional modifications (IL-1, TNFalpha), release certain pituitary hormones and inhibit others (much of which is indicated in the graph reproduced from his article), promote general catabolism, (mediated primarily by TNF-alpha, also known as cachectin), stimulate the production of new serum proteins known as acute phase reactants in the liver (the joint action of IL-6, glucocorticoids and catecholamines), and also elevate the production of leucoytes in the bone marrow, the mechanism of which is not fully elucidated. (For further reference, please see also the papers by Asa and Kovacs, Besedovsky and del Rey, Gaillard, and Nagy and Berczi in this volume.) Thus, with the recent discovery of cytokines and our increasing recognition of their functions, we have begun to fill in the gaps in Dr. Selye's adaptation syndrome outlined nearly half a century ago.
In 1949 Selye discovered that an inflammatory reaction, which can be induced in the rat by the parenteral administration of egg white, is inhibited by cortisone or by purified ACTH. On the other hand, desoxycorticosterone acetate, a mineralcorticoid compound, tends to aggravate the reaction. These experiments initiated his interest in inflammation which became the most lasting topic in his research and led to the proposition later that diseases, like rheumatoid arthritis, anaphylaxis, etc. are in fact diseases of adaptation as stated in numerous publications.
"Among the derailments of the general adaptation syndrome that may cause disease, the following are particularly important:
(i) an absolute excess or deficiency in the amount of adaptive hormones (for example, corticoids, ACTH, and STH) produced during stress; (ii) an absolute excess or deficiency in the amount of adaptive hormones retained (or `fixed') by their peripheral target organs during stress; (iii) a disproportion in the relative secretion (or fixation) during stress of various antagonistic adaptive hormones (for example, ACTH and antiphlogistic corticoids, on the one hand, and STH and prophlogistic corticoids, on the other hand); (iv) the production by stress of metabolic derangements, which abnormally alter the target organ's response to adaptive hormones (through the phenomenon of `conditioning'); and (v) finally, we must not forget that, although the hypophysis-adrenal mechanism plays a prominent role in the general-adaptation syndrome, other organs that participate in the latter (for example: nervous system, liver, and kidney) may also respond abnormally and become the cause of disease during adaptation to stress.
Corticoid requirements during stress:During stress, the corticoid requirements of all mammals are far above normal. After destruction of the adrenals by disease (as after their surgical removal), the daily dose of corticoids, necessary for the maintenance of well-being at rest, is comparatively small, but it rises sharply during stress (for example: cold, intercurrent infections, and hemorrhage), both in experimental animals and in man.
Anti-inflammatory effects of corticoids: The same antiphlogistic corticoids (cortisone and cortisol) that were shown to inhibit various types of experimental inflammations in laboratory animals exert similar effects in a human being afflicted by inflammatory diseaes (for example, rheumatoid arthritis, rheumatic fever, and allergic inflammations). "Sensitivity to infection after treatment with antiphlogistic corticoids. In experimental animals, the suppression of inflammation by antiphlogistic hormones is frequently accompanied by an increased sensitivity to infection, presumably because the encapsulation of microbial foci is less effective and perhaps partly also because serologic defense is diminished.
Psychological and psychiatric effects of corticoid overdosage: It has long been noted that various steroids - including desoxycorticosterone, cortisone, progesterone, and many others - can produce in a variety of animal species (even in primates such as the rhesus monkey) a state of great excitation followed by deep anesthesia. It has more recently been shown that such steroid anesthesia can also be produced in man, and, of course, the marked emotional changes (sometimes bordering on psychosis) that may occur in predisposed individuals during treatment with ACTH, cortisone, and cortisol are well known. Several laboratories reported furthermore that the electroshock threshold of experimentl animals and their sensitivity to anesthetics can be affected by corticoids."
The prediction by Selye that the pituitary gland has the capacity to both stimulate and inhibit inflammatory reactions is the subject of recent investigations and is proven correct. The notion of prophlogistic steroids has not been studied to a great extent to date, but the antiinflammatory effect of glucocorticoids is firmly established and it is clear today that the adrenal gland plays an important physiological role in the regulation of immune and inflammatory responses. The disproportion of hormones and other mediators, altered responsiveness in tissues and the significance of metabolic derangements during acute phase reactions related to sepsis, severe trauma and shock are the subject of current investigations and deemed to be highly relevant to prognosis. The involvement of the central nervous system, the liver and of other organs, such as the kidney, is also substantiated. That "conditioning" may also play a role in host defence is also gaining ground. Some hard evidence is forthcoming regarding the corticoid requirements during infection and other forms of stress. The antiinflammatory effect of cortisone and cortisol are well recognized and are widely applied in medicine today. That corticosteroids increase the sensitivity to infection is of common knowledge. The phenomenon of stress related anesthesia is well recognized, but opioid peptides rather than steroid hormones are considered to be the mediators.
P-selectin- and CD18-mediated recruitment of canine neutrophils under conditions of shear stress
Neutrophil mobilization at sites of inflammation or thrombosis involves the participation of several adhesion molecules expressed on neutrophils and vascular endothelial cells. Local vascular damage with disruption of the endothelium results in adhesion of platelets to the exposed subendothelium, and these platelets could also participate in neutrophil recruitment. This initial phase of mobilization could be followed by heterotypic aggregation to recruit more leukocytes in the area. The present study first examined the interactions of adherent canine platelets and flowing canine neutrophils using an in vitro system that simulates vascular flow conditions. Results showed that collagen-adherent platelets express the adhesion molecule P-selectin on their surface and can support neutrophil arrest (612 +/- 43 neutrophils/mm2) at shear stresses of approximately 2.5 dynes/cm2. Both transient adhesion (manifested by a rolling-type behavior) and complete arrest were observed. These interactions could be totally inhibited by a monoclonal antibody directed against platelet P-selectin (24 +/- 18 neutrophils/mm2) but not by a monoclonal antibody against neutrophil CD18 (625 +/- 46 neutrophils/mm2). Additionally, under shear mixing conditions (700 RPM), canine blood leukocytes exhibited aggregation (> 80% singlets recruited into aggregates after 5 minutes), and this process does not involve P-selectin but is dependent on the neutrophil integrin CD18. However, stimulation of the blood with platelet-activating factor (5-20 ng/ml) induced a rapid aggregation with a significantly greater number of aggregates when compared with stirring alone (68.3% +/- 3.2% versus 35.2% +/- 6.3% at 1 minute, P < 0.05), and this aggregation was both P-selectin and CD18 dependent. Overall, these two mechanisms of leukocyte recruitment (neutrophil arrest on adherent platelets and aggregation) could act sequentially and in a cooperative manner to bring into close contact platelets and neutrophils at sites of inflammation and thrombosis in pathologic conditions in the dog.
Measuring stress in captive animals.
Stress is rarely thought to be a good thing, but is it true that all stress is necessarily bad? In the animal kingdom, such disparate events as mating, fighting, or hunting can trigger an animal's stress response.
Stress is a normal part of life, but what isn't so obvious, especially for zoologic institutions, is determining whether a captive animal is experiencing the good kind of stress that helps keep it alive or the harmful kind.
In her Oct. 11 AVMA Animal Welfare Forum presentation "Stress and distress: evaluating their impact for the well-being of zoo animals," Nadja Wielebnowski, PhD, a behavioral endocrinologist at Chicago's Brookfield Zoo, discussed some of the studies under way to measure stress in captive animals.
"Not all stress is negative, and some stressful situations, like exploring a new element in the environment or mating, usually are seen as beneficial and can help reduce animal boredom in captivity," Dr Wielebnowski said.
"In zoos, we are most concerned with chronic stress, when animals are repeatedly exposed to negative stressors and are not able to respond appropriately. Prolonged negative stress can become physically harmful."
Researchers at Brookfield Zoo are currently studying stress in 18 species using techniques that may be expanded and applied to more species. The procedure includesdaily collecting, testing, and validating of fecal samples for used hormone analysis along with extensive monitoring of behavioral and physiologic changes.
Brookfield's clouded leopard collection is part of a national study started in 1999 involving 12 zoos and 74 large cats. Difficult to manage in captivity, clouded leopards are often seen pulling out their fur, pacing excessively, hiding for long periods, and acting aggressively toward exhibit mates.
Research has shown that higher-than-average concentrations corticosteroids in the feces--an indicator of stress--are positively correlated with the occurrence of self-injuring behaviors, as well as the frequency of pacing and hiding.
In addition, when husbandry factors were analyzed, it was found that enclosure height, keeper time, being able to see potential predators, and public display were all associated with hormonal changes. The higher the enclosure, for example, the lower the hormone concentrations.
The Clouded Leopard Species Survival Plan Committee of the American Zoo and Aquarium Association has already recommended increasing enclosure height to a minimum of 10 to 12 feet for this big cat species.
"Zoos have made great progress in animal welfare over the past several decades," Dr. Wielebnowski said, "but there is still work to be done. We need to identify more accurate and reliable scientific measurements to increase our understanding of what well-being means from the individual animal's point of view. This includes species as different as the charismatic polar bear to the hissing cockroach."
ASPCA study finds cocoa bean mulch could harm dogs
The American Society for the Prevention of Cruelty to Animals' Animal Poison Control Center is warning dog owners about the dangers of cocoa bean mulch.
A retrospective study of case data collected by the center from January 2002 to April 2003 found that dogs that consumed cocoa bean shell mulch might have signs consistent with methylxanthine toxicosis, which is similar to those seen with chocolate poisonings.
The center presented its findings at the North American Congress of Clinical Toxicology in September.
Data suggest the most common signs that occurred following ingestion were vomiting and muscle tremors. Although it wasn't possible to quantify exact amounts involved in these adverse events, anecdotal evidence appears to indicate that the severity of clinical signs increases when larger amounts are ingested.
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