[Studies on inhibitory mechanism of insulin secretion associated with open-heart surgery (author's transl)].
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Biomedical subjects
Publications and source records attributed to H Shida.
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The present studies were performed to evaluate the protective effect of topical hypothermia on anoxic heart. The myocardial protection was assessed by myocardial contractility in the isolated blood-perfused electrically driven canine left ventricular muscle. The isometric tension and the rate of rise of tension development (dT/dt) were measured before and after hypothermic anoxic arrest and percent recovery of these values was used as a parameter of myocardial contractility. The percent recovery rates of 100, 95, 90, and 65 were obtained after acute anoxia of 90, 120, 150, and 180 min, respectively at the myocardial temperature of 17 degrees C. These data suggest that the safe limit of acute anoxia at the myocardial temperature of 17 degrees C is defined as 90 min in this experimental model and it can be extended to 120 min at the myocardial temperature below 17 degrees C.
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The role of the liver in the changes of acid-base balance and plasma lipids in surface-induced deep hypothermia for open-heart surgery was investigated clinically and experimentally. The metabolic acidosis generally observed in open-heart surgery under surface-induced deep hypothermia is derived from lactacidemia. Although the accelerated anaerobic glycolysis is partly responsible, the depressed acidic metabolite-disposing ability of the liver also plays an important role. The evidence which is presented to show the decrease of plasma lipids other than NEFA under hypothermia is probably due to the hepatic accumulation of lipids and the decreased lipids release from the liver.
Plasma lipids, blood glucose, plasma insulin (IRI) and serum dopamine-beta-hydroxylase (DBH) were measured in 30 subjects undergoing surface-induced deep hypothermia with circulatory arrest for open-heart surgery. Non-esterified fatty acid (NEFA) in the plasma rapidly increased at the lowest temperature (23 degrees C) reached and other lipids in the plasma decreased during the cooling period. An increase of NEFA and a decrease of triglyceride have been attributed to the action of lipoprotein lipase activity stimulated by heparin. It is also likely that the decrease of other lipids and beta-lipoprotein in the plasma results from the transient hypofunction of the liver due to hypothermia. Blood glucose increased during the cooling period, while plasma insulin showed no significant change. Serum DBH reflecting catecholamine also showed no significant change during the cooling or rewarming periods. Therefore, hyperglycemia in hypothermic open-heart surgery may result from the decrease of peripheral utilization of glucose and from the inhibition of insulin secretion due to the transient pancreatic hypofunction.
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In surface-induced deep hypothermia, metabolic acidosis resulting from lactacidemia was observed. In the aspect of myocardial metabolism, the rate of reduction in coronary A-V difference ratio of lactate, pyruvate and NEFA was less than that of coronary flow and myocardial oxygen consumption in the hypothermic heart. Namely, it seems that lactate, pyruvate and NEFA play an important role as energy fuel in the hypothermic heart. On the other hand, myocardial metabolism of glucose was reduced in the hypothermic heart. Moreover, it seems that exogenous corticosteroid and ATP do not influence on the myocardial metabolism of carbohydrate and lipid in the hypothermic heart.
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