Other potentially misleading findigs at necropsy of young dogs and horses include diffuse or patchy myocardial pallor that

subsequently fails to correlate with any detectable microscopic alterations .Also ,the intracardiac injection of euthanasia solution and other substances can cause hemopericardium and myocardial pallor from tissue dissolution and from crystalline deposists at the site of solution deposition. Cardiac muscle cells are surrounded by interstitial components,which include blood and lymph vessels, nerves,and connective tissue cells such as fibroblasts, histiocytes,mast cells,pericytes,primitive mesenchymal stem cells and extracellular matrix elemnts of connective tissue,including collagen fibrils,elastic fiers,and acid mucopolysaccharides.Cardiac muscle cells can be divided into two populatiions the workimg myocytes and the specialized fibers of the condution system.The working myocyte is a cross-striated branching fiber of an irregular cylindrical shape that measures 60 to 100 ,in length and ,in diameter, with centrally located, elongated nuclei.Myocytes in young animals are smaller and have small amounts of sarcoplasm.Artrial myocytes are smaller than ventricular myocytes.Adjacent myocytes are joined end-to end by specialized junctions known as intercalated disks and less frequently by side-to-side connections termed lateral junctions.Multinucleated fibers with nuclei arranged in central rows are frequently seen in hearts of growing pigs. 63- that stem cells exist in adult animal and human hearts and,with myocardial injury,these cells may differentiate into cardiac muscle cells.However, the extent of myocyte regeneration is probably minimal.Hyperplasia of myocytes is a normal componenet of cardiac growth in the first several months of life. Then proliferation ceases.normal growth then is the result of hypertrophy of myocytes until cell sizes normal for th species are reached. Apoptosis(programmed cell death of myocytes) is incressingly recognized for its role in the development of various myocardial lesions and cardiac diseases.These conditiond include cardiac development.ischemic injury.several types of experimentally induced heart failure(ischemiareperfusion ,hypoxia, pressure-overload hypertrophy),and cardiotoxicity.In some cell systems,apoptosis can be triggered by the presence of excessive amounts of oxygen free redicals.Cells dying by apoptosis shrink and from apoptotic bodies.In contrast to cell death by necrosis,apoptosis is not accompanied by an inflammatoru reaction on fibrosis. Histopathologic study of fsections of the myocardium is substantially limited in respect to specific diagnoses and only rarely can an etiologic diagnosis be made from the morphologic alterations. This inadequacy exists because the spectrum of fpathologic reactions is a limited one,and many agents that damage the heart produce similar lesions.Myocardial necrosis can be confused with myocardial inflammation with secondary necrosis because both lesions have dubstantial leukocytic infiltration.Some animals that die peracutely from cardiac failure lack detectable microscopic alterations and are presumed to have sufferes from an arrhythmic episode resulting in syncope.Hearts with long-standing myocardial damage have foci of fibrosis,regardless of the cause

of the loss of myocytes.correlation between the severity of clinical cardiac disease and the severity of myocardial injury can be poor: a small lesion at a critical site,such as a portion of the conduction system can be fatal,whereas a widespread myocardial lesion.such as myocarditis,can be asymptomatic. Cardiac Pathophydiology The results of normal cardiac function include the maintenance of adequate blood flow called cardiac output to peripheral tissues that provide delivery of oxygen and nutrients, the removal of carbon dioxide and other metabolic wasre products,the distribution of hormones and other cellular regulators,and the maintenance of adequate thermoregulation and glomerular filtration pressure (urine output).The normal heart has a threefold to fivefold functional reserve capacity, but this capacity can eventually be lost in cardiac disease and the result is impaired fuction. Compensatory mechanisms operate in both normal and diseases hearts in an attempt to meet both the short-term and long-term demands for adequate cardiac output.These mechanisms include cardiac dilation, myocardial hypertrophy,increase in blood volume,and redistribution of blood flow.These compensatory mechanisms can maintain cardiac output that is adequate for some time , even in animals with rather severe cardiac disease sufficient to compromise cardiac function from loss of myocardial aontractility,sustained pressure overload,or sustained volume overload. Cardiac delation can occur as a terminal lesion in many cardiac diseases.As a compensatory response to archive increased cardiac output,dilation allows stretching of cardiac muscle cells to increase contractile force according to the Frank-Starling