Myocardial Lactate and Pyruvate Metabolism*

Abstract

Although the heart has been considered primarily an aerobic organ, recent work (1) has reemphasized the possibility that measurement of oxygen consumption alone may not 1)e adequate to define the total energy utilization under all conditions. The role of anaerobic metabolism must be reviewed.Methods of defining as well as quantifying anaerobiosis are currently in dispute. When oxidation and glycolysis proceed at the same rate, carbohydrate is oxidized to CO2 and H20. Lactate arises whenever the rate of glycolysis exceeds the rate of oxidation. Net production of lactate by an organ, as evidenced for example by venous concentration greater than arterial, has been considered to represent anaerobic metabolism due to cellular hypoxia (2). More recent work (3) has demonstrated that large changes in lactate production can occur unassociated with hypoxia, but related instead to increased pyruvate production. Huckabee introduced the concept of "excess lactate" in order to distinguish between pyruvateinduced changes in lactate and those related solely to a shift in DPN: DPNH redox potential. This was inferred from alterations in arterial lactatepyruvate ratio and the relative arteriovenous differences of the two substrates. "Excess lactate," so defined, was considered an indicator of cellular oxygenation and was used quantitatively as a measure of anaerobic metabolic rate.Anaerobic metabolism in cardiac muscle has been considered to occur only under extreme conditions. Whereas earlier work (4-9) showed lactate production only sporadically with stresses of hypoxia, shock, or myocardial emboli, Huckabee (1) found that in dogs the stress of either 10 per cent oxygen breathing or leg exercise would result in myocardial excess lactate despite positive

Hemodynamics, coronary blood flow, and myocardial metabolism in coronary shock; response to l-norepinephrine and isoproterenol

“…Huckabee and associates suggested that production of lactate in excess of pyruvate, "excess lactate," was a sensitive indicator of myocardial hypoxia (39). Results of animal and clinical research have emphasized that myocardial lactate production alone is a reliable indicator of anaerobic metabolism (65)(66)(67)(68)(69)(70)(71)(72) while lactate extraction less than 10% is suggestive of myocardial hypoxia (65). An increased lactate to pyruvate ratio in the coronary sinus compared to arterial blood is believed indicative of inadequate myocardial metabolism (73)(74)(75).…”

Regional Myocardial Perfusion Rates in Patients with Coronary Artery Disease

“…Indirect evidence has been provided by animal experiments in which reduction of the coronary blood supply to areas of left ventricle reduced myocardial oxygen consumption, reversed the normal myocardial extraction of lactate from arterial blood, and depressed ventricular function (2)(3)(4). Studies in patients with arteriographically demonstrable coronary lesions have shown increased extraction of oxygen from the coronary circulation (5), increased levels of lactate in coronary venous blood (6), and local abnormalities of ventricular wall contraction during induced angina pectoris (7).…”

Effects of ouabain on myocardial oxygen supply and demand in patients with chronic coronary artery disease. A hemodynamic, volumetric, and metabolic study in patients without heart failure.

“…Oxygen content was determined from P02, PH, and hemoglobin using a Severinghaus nomogram (20) and assuming a normal hemoglobin-oxygen dissociation curve. Serum lactate was measured by a modification of the enzymatic method of Horn and Bruns (21,22). Myocardial oxygen consumption was calculated as the product of coronary blood flow and arterial-coronary venous oxygen difference ({A-CV}02 difference).…”