Effect of glucose-insulin-potassium infusions on arteriovenous differences of glucose of free fatty acids and on tissue metabolic changes in dogs with developing myocardial infarction.

Glucose-insulin-potassium infusions were given to dogs for 6 hours, starting 30 minutes after ligation of the left anterior descending coronary artery. Effects on substrate arteriovenous differences, indexes of ischemic damage and other tissue metabolic changes were compared with changes in dogs with comparable ligations but no infusions. Glucose-insulin-potassium increased the arteriovenous difference of glucose, decreased that of free fatty acid and decreased the arterial free fatty acid/albumin molar ratio. Glucose-insulin-potassium accelerated the rate of fall of the epicardial S-T segment in the infarct zone and prevented the small rise in S-T segment found in the perlinfarct and nonischemic zones. Glucose-insulin-potassium increased the tissue content of glycogen in peripheral infarct, periinfarct and nonischemic zones; increased tissue potassium ion/sodium ion ratios in epicardial infarct zones and in the periinfarct zone; increased adenosine triphosphate in the endocardial infarct zone; decreased inorganic phosphate in the periinfarct and nonischemic zones and in the endocardial infarct zone; and increased lactate in the central infarct and nonischemic zones. The phosphate potential increased in the periinfarct and nonischemic zones. Thus, many glucose-insulin-potassium effects were greater in the peripheral infarct and especially the periinfarct zones. Although increased anaerobic metabolism with lactate production could not be excluded as a mode of action of glucose-insulin-potassium, estimated rates of anaerobic glycolysis were very low, suggesting that other effects such as increased aerobic glycolysis decreased extraction of free fatty acid by the heart, increased tissue glycogen or a "membrane" effect might be of major importance.