Pretto E, Schaible T, Scheuer J, Safar P, Stezoski S W
Crit Care Med. 1986 Jun;14(6):560-2. doi: 10.1097/00003246-198606000-00009.
Perfusion of isolated, nondiabetic rat hearts with high concentrations of regular insulin (10 mU/ml) produced earlier onset of myocardial contracture during ischemia than control perfusions without insulin. High insulin concentrations also increased total myocardial calcium content (p less than .001) and myocardial Ca-45 uptake postischemia (p less than .05). Insulin perfusion before ischemia did not enhance calcium uptake. These results support the hypothesis that insulin may increase calcium movement across myocardial cell membranes, which may lead to increased ischemic contracture. Insulin-aggravated myocardial ischemia in cardiothoracic surgery and cardiac resuscitation deserves further investigation.
用高浓度常规胰岛素(10 mU/ml)灌注分离的非糖尿病大鼠心脏,与无胰岛素的对照灌注相比,缺血期间心肌挛缩的发作更早。高胰岛素浓度还增加了心肌总钙含量(p <.001)和缺血后心肌Ca-45摄取(p <.05)。缺血前的胰岛素灌注并未增强钙摄取。这些结果支持以下假设:胰岛素可能增加钙跨心肌细胞膜的转运,这可能导致缺血性挛缩增加。胰岛素加重心胸外科手术和心脏复苏中的心肌缺血值得进一步研究。