Abstract

To define the mechanism of the cardiodepressant action of halothane, we used the perfused working rat heart to study the effects of the anesthetic on glucose utilization and left ventricular function, both in the absence and presence of insulin. Rates of glucose utilization were measured by the appearance of 3HOH in the coronary effluent derived from 2-3H-glucose added to the media. Lactate production was determined by enzymatic methods. Tissue glycogen was measured by enzymatic methods to calculate total glucose available for energy production by the heart. Halothane, up to 2.4% concentration, had a dose dependent depressant effect on oxygen consumption, mechanical performance, and utilization of media glucose. Exogenous insulin did not affect this relation. Glycogen stores decreased in the presence of halothane and control values were not preserved by the presence of insulin. Lactate production was depressed by halothane in the absence of insulin and was unchanged in the presence of insulin. The ratio of glycolysis to oxygen consumption was increased by halothane both in the presence and absence of insulin. This disparate effect on glucose metabolism, compared with function, may be explained by an inhibition of pyruvate dehydrogenase.

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