Abstract

The value of measurements of lactate in coronary venous blood as a sign of myocardial anaerobiosis is reassessed. Lactate was measured after coronary arterial ligation in dogs in (1) local venous blood draining from ischemic tissue, (2) coronary sinus blood, and (3) myocardial tissue. There was an estimated lactate concentration gradient of 2- to 4-fold from ischemic tissue (epicardial biopsy specimens) to local venous blood, whereas the gradient from epicardial tissue to coronary sinus blood was 8- to 16-fold. Differences in pyruvate concentrations between ischemic tissue and local venous or coronary sinus blood were not marked. Increases in tissue lactate concentration and in lactate/pyruvate values in anaerobic tissue occurred simultaneously. Whether such tissue changes are reflected in coronary venous blood depends on the degree to which the heart cell membrane impairs egress of lactate or pyruvate, and on the venous sampling site. With coronary sinus sampling, the production of small ischemic lesions (less than 10 percent of the volume of the whole heart) caused a readily detected decrease of lactate extraction by the heart, whereas the changes in the lactate/pyruvate ratio across the heart were less marked. When lesions were larger or when highly selective coronary venous sampling techniques were used, lactate/pyruvate changes were readily detectable; changes in the ratio beta-hydroxybutyrate/acetoacetate were not very helpful in detecting ischemia. Although lactate changes in coronary venous blood are a very sensitive index of regional myocardial ischemia after coronary arterial ligation, a knowledge of changes in lactate/pyruvate ratios, potassium ion, inorganic phosphate and hydrogen ion allows a more complete description of intracellular events. These additional measurements should also help to exclude unusual circumstances in which lactate discharge from the heart occurs in the presence of apparently normal oxygenation.

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