Effects of prolonged coronary hypotension on myocardial substrate utilization.
Myocardial substrate utilization was investigated following experimental coronary hypotension in isolated in vitro perfused dog hearts. Control observations were made at the beginning and at the end of the experiments with afterload of 100 mm Hg. Between the two controls, the afterload was lowered to 50 mm Hg and kept at that level for 4 hours. The observations during the hypotensive period were compared to the two controls. Lactate uptake and the percentage contribution of the lactate to myocardial CO2 production were diminished during the hypotensive period. Myocardial free fatty acid (FFA) uptake and oxidation did not change significantly. Glucose uptake and myocardial respiratory quotient (RQ) were decreased. Thus, prolonged coronary hypotension caused a relative preference of FFA oxidation and diminished lactate and glucose uptake by the myocardium. It is of interest to note that these changes in substrate utilization were quite different from those observed during experimentally produced hemorrhagic hypotension or endotoxic shock.
D000818:Animals; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology; D007022:Hypotension / Q000150:complications / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D012769:Shock / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D007773:Lactates; D005947:Glucose