Effect of hypothermia of 25 C for 24 hr was determined on myocardial metabolism and efficiency in dogs fasted for approximately 15 hr and anesthetized with sodium pentobarbital. Coronary blood flow, cardiac output, myocardial oxygen and substrate utilization, and mechanical efficiency of the heart were determined at normal and reduced body temperatures. Prolonged reduction of myocardial temperature with concomitant reduction in coronary blood flow led to diminished oxygen and substrate utilization. Myocardial glycolysis began after 12 hr of cooling when pyruvate utilization stopped in negative balance. After 24 hr the heart stopped utilizing carbohydrates with negative arteriovenous differences for these substrates (in the presence of normal arterial carbohydrate levels), but continued to utilize nonesterified fatty acid. The coefficient of oxygen utilization for the heart increased following 24 hr of cooling, suggesting a relative state of myocardial hypoxia. The appearance of hypoxia and glycolysis during the late hours of cooling suggests that the limit of tolerance of the heart to cooling was near.
The changes occurring in cardiac output and oxygen consumption in short periods of hypothermia are the same when either ether or pentobarbital sodium is used as the anesthetic agent during the induction of hypothermia. Following an initial decrease in oxygen consumption, no further change occurred as long as the body temperature was maintained at a constant level. Cardiac output, arterial-venous oxygen difference, and coefficient of oxygen utilization remain unchanged for longer periods of time than most physiologic parameters studied during prolonged hypothermia at constant temperatures. After about 14 hours they also begin to alter so that by 24 hours the changes are profound. Stagnant anoxemia and marked increased in the coefficient of O2 utilization resulting from the markedly lowered cardiac output, which was 5% of the precooled controls, occurred.
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