Myocardial lactate oxidation in situ and the effect thereon of reduced coronary flow

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Abstract
A tracer method based on the production of C14O2 from lactate-1-C14 was devised for estimating the rate at which blood lactate undergoes oxidative decarboxylation in the myocardium of the open-chest dog when blood flow to the cannulated main left coronary is at control or reduced rates. Under control conditions, an average value of 31.4 [plus or minus] 10.9 [mu]M/100 g/min. was obtained, which closely approximated that of net myocardial lactate uptake. Complete oxidation of this amount of lactate accounted for 24. 7% of the O2 consumed by the myocardium. When coronary flow was mechanically reduced to insufficiency levels, oxidative decarboxylation of lactate peristed at 14. 9[plus or minus]5.1 [mu]M/100 g/min. at a time when the arterio-coronary sinus lactate difference revealed net myocardial lactate production. Pyruvate uptake and coronary sinus pH were reduced. These findings suggest that the primary metabolic fate of lactate entering the myocardium is oxidation, and that when left coronary flow is sufficiently reduced, aerobic and anaerobic metabolism occur simultaneously in different regions of the contracting myocardium.

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