Effects of coronary hypotension on myocardial substrate utilization.
Changes in myocardial substrate utilization were studied after experimental coronary hypotension in the isolated dog heart perfused with the blood of a large donor animal. After a control period (100 mmHg) the afterload of the isolated heart was adjusted to 50 mmHg and kept at that level for 4 h. After this period, a second control observation was made at a 100-mmHg afterload. Coronary sinus blood flow and oxygen consumption decreased during hypotension and returned to normal during the second control period. Myocardial free fatty acid (FFA) uptake and oxidation did not change significantly. Lactate uptake and the percentage of CO2 derived from myocardial lactate utilization were both diminished during hypotension. These changes were not present during the second control period. Glucose uptake and myocardial respiratory quotient were decreased during the hypotensive period. Half the hearts exhibited elevated end-diastolic pressure after hypotension, but no metabolic differences were detectable between the failing and nonfailing hearts. Thus, prolonged severe hypotension caused a relative preference of FFA oxidation and diminished lactate and glucose uptakes by the myocardium. These changes were quite different from those obtained during experimental hemorrhagic or endotoxic shock.
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D003326:Coronary Circulation; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006339:Heart Rate; D007022:Hypotension / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D012039:Regional Blood Flow
D005230:Fatty Acids, Nonesterified; D007773:Lactates; D002245:Carbon Dioxide; D005947:Glucose