Effect of hypothermia on myocardial metabolism

Abstract

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.

Serum Enzyme Levels During Experimental Hypothermia in Man

“…In experimental animals, large reductions of deep body temperature (TDB) lead to elevations of the levels in the serum of enzymes associated with tissue damage [Blair, Hook, Tolly and Bunce, 1961;Russ and Lee, 1965;Zimny and Taylor, 1965]. This response is also seen in human patients in hypothermia artificially induced for surgical procedures [Rehn, Kohnlein and Brintzinger, 1961;Atanasov, 1965;Kingsley, 1966] and in accidental hypothermia [Duguid, Simpson and Stowers, 1961;Prescott, Peard and Wallace, 1962;Maclean, Griffiths and Emslie-Smith, 1968;Maclean, Murison and Griffiths, 1974].…”