Insulin worsens ischemia-induced myocardial contracture in the isolated rat heart.
We used a modification of Langendorff's isolated perfused nonworking rat-heart model to study the effects of diabetes, insulin-treated diabetes, and hyperinsulinemia on left ventricular pressure, force of ventricular contraction, and myocardial contracture, before, during, and after 20 min of complete normothermic global ischemia. Untreated diabetic rat hearts behaved the same as normal hearts, but insulin-treated diabetic hearts had more ischemic and postischemic contracture (p less than .01), and less return of left ventricular function. Chronic insulin treatment potentiated ischemic contracture in diabetic and nondiabetic rat hearts. These results support the hypotheses that insulin can increase Ca++ actin-myosin ATPase activity, and increase the affinity of myofibrillar receptors for calcium, which may lead to increased ischemic contracture. Insulin as a risk factor in myocardial ischemia, cardiothoracic surgery and cardiac resuscitation, and other pathogenetic factors of "stone heart" development, deserve further investigation.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000503:physiopathology*; D006946:Hyperinsulinism / Q000503:physiopathology; D066298:In Vitro Techniques; D007328:Insulin / Q000633:toxicity*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D011292:Premedication; D051381:Rats; D011919:Rats, Inbred Strains; D012306:Risk
D001786:Blood Glucose; D007328:Insulin