HYPERINSULINEMIA INDUCES MYOCARDIAL INFARCTIONS AND ARTERIOLAR MEDIALHYPERTROPHY IN SPONTANEOUSLY HYPERTENSIVE RATS

To investigate the effects of hyperinsulinemia on the myocardial vesse ls, long acting insulin (mixtard, a combination of 30% regular human i nsulin and 70% NPH human insulin) was injected daily for 8 weeks, intr aperitoneally, in two strains of rats, normotensive WKY and hypertensi ve SHR. There were four groups in all, a control group, and an insulin -injected group in each strain. The drinking water contained 10% gluco se to prevent hypoglycemia in the insulin-injected rats. At the end of the 8 weeks experimental period, after measuring blood pressure and t aking blood for the determination of glucose, urea, creatinine, and in sulin, the rats were killed. The organs were fixed in formaldehyde. Th e blood glucose levels were higher at the end of the experiment, in bo th the placebo- (saline)-injected and the insulin-injected rats. Blood pressure rose significantly only in the insulin-injected SHR. The int ramyocardial arterioles in the insulin-injected SHR had a significantl y thicker vascular wall than the placebo-injected SHR, as represented by the vessel wall to lumen ratio, because of hypertrophy of the media . When compared with the placebo injected WKY rats, there was a higher wall/lumen ratio of the intramyocardial arterioles in the insulin-inj ected WKY, but the difference did not reach significance. Heart weight s factored by body weights was significantly higher in insulin-injecte d as compared with placebo-injected SHR. Myocardial infarctions were o bserved in four of eight rats in the insulin-injected SHR group despit e the fact that there were no signs of atherosclerosis or intimal thic kening. It is possible that the increase in heart weight and the proba ble increase in metabolic activity resulting from hyperinsulinemia, to gether with the increased oxygen demand of the myocardium and the arte riolar narrowing, may have contributed to the occurence of myocardial infarctions in the absence of atherosclerotic coronary occlusion. (C) 1997 American Journal of Hypertension, Ltd.