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Following experimental myocardial infarction in the dog elevations of serum levels of glutamie-oxaloacetic transaminase (SGO-T), glutamic-pyruvic transaminase (SGP-T) and lactic dehydrogenase (SLID) were consistently noted in decreasing order. Evidence is presented that leakage into the serum from the damaged myocardium plays an important role in these elevations. This concept is supported by analyses of original tissue to blood enzyme concentration gradients, activities of homogenates of infarcts of varying ages, simultaneous measurements of eoronary sinus and peripheral venous blood following infarction and contrasting results in man and the dog following infarction. C LINICAL or experimentally induced myocardial necrosis is consistently associated with rises in the serum activity of the enzyme, glutamie-oxaloacetic transaminase. 1 ' -It appears that these alterations result in part from leakage of the enzyme from the neerotic heart muscle into the serum. The alterations in activity of glutamie-oxaloacetic transaminnase in the serum (SGO-T) are roughly proportional to the extent of myocardial necrosis. 2 Reversible myocardial damage without necrosis, such as that seen in coronary insufficiency and pericarditis, does not appreciably influence the serum activity of the enzyme.Studies of the activity of lactic dehydrogenase and glutamic pyruvic transaminase (SLD, SGP-T)-4 ' 8 -9 as well as of SGO-T in the serum after heart muscle damage also suggested that these enzymes were released from the neerotic muscle resulting in serum activity variations proportional to the original gradients in concentration between the intact

Previous studies have demonstrated consistent rises in serum activity of the enzyme, glutamic oxaloacetic transaminase (SGO-T), following myocardial necrosis of various etiologies. The present study demonstrates markedly different findings in experimental and clinical coronary insufficiency, pericarditis, and pulmonary infarction unless concomitant myocardial necrosis was present. This seems to be a valuable means of differentiating clinical problems in which the presence of myocardial injury is suspected as the basis of the patient's chest pain.

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