Jackson C V, McGrath G M, Tahiliani A G, Vadlamudi R V, McNeill J H
Diabetes. 1985 Sep;34(9):876-83. doi: 10.2337/diab.34.9.876.
The effects of experimental diabetes on cardiac function and ultrastructure were studied in rats that had been diabetic for 6-24 wk. Experimental diabetes was produced by the intravenous (i.v.) injection of 65 mg/kg streptozocin (STZ) into rats 42-43 days old. Diabetic rat hearts perfused at 15 cm H2O on the working heart apparatus demonstrated depressed cardiac function (i.e., lower left ventricular pressure and +/- dP/dt) at 6, 12, and 24 wk of diabetes. Electron microscopic analysis of ventricular myocardium revealed increased lipid deposition from 6 to 24 wk of diabetes and progressive deterioration of the myocardial cell integrity at 12 and 24 wk of diabetes. This deterioration was characterized by loss of contractile protein, vacuolization (swollen sarcoplasmic reticulum), myelin formations, myocytolysis, and contracture bands. These alterations paralleled the depression of cardiac function at 12 and 24 wk of diabetes. There was, however, depressed function at 6 wk of diabetes but no observable alterations in myocardial ultrastructure. Therefore, experimental diabetes produced ultrastructural alterations in the rat heart that manifested themselves only after a demonstrable depression in cardiac function.
在糖尿病病程为6 - 24周的大鼠中研究了实验性糖尿病对心脏功能和超微结构的影响。通过给42 - 43日龄的大鼠静脉注射65 mg/kg链脲佐菌素(STZ)诱导实验性糖尿病。在工作心脏装置上以15 cm H₂O灌注糖尿病大鼠心脏,结果显示在糖尿病病程6周、12周和24周时心脏功能受到抑制(即左心室压力及±dP/dt降低)。对心室心肌进行电子显微镜分析发现,糖尿病病程6周至24周时脂质沉积增加,在糖尿病病程12周和24周时心肌细胞完整性逐渐恶化。这种恶化的特征为收缩蛋白丢失、空泡化(肌浆网肿胀)、髓鞘形成、心肌溶解和挛缩带。这些改变与糖尿病病程12周和24周时心脏功能的抑制情况平行。然而,糖尿病病程6周时心脏功能受到抑制,但心肌超微结构未观察到明显改变。因此,实验性糖尿病导致大鼠心脏超微结构改变,这些改变仅在心脏功能出现明显抑制后才表现出来。