Maeda S
Acta Pathol Jpn. 1980 Jan;30(1):59-78.
Radiation-induced heart injuries were morphologically studied by using the rabbits irradiated with a single dose of 3,000R (group I) or 300R of X-ray group II) from 1 hour until 6 months. There was no essential difference in the lesions of the hearts from group I and that of group II. Acute epicarditis was found as early as 1 hour after irradiation and it became maximum in severity at 1-2 days. In the myocardium, there were degeneration and resolution of the myocardial cell, various architectural changes of mitochondria, and disorganization of the intercalated disc. Polymorphonuclear cell infiltration and endothelial injuries of the capillaries occurred in the interstitial tissue. In addition, endocarditis with or without thrombus formation was often found. Acute inflammation was seen in the myocardium of group II rather later than that of group I, but it disappeared earlier. In the later stage, fibrosis finally occurred in the epicardium and endocardium. Glycoprotein degeneration of the muscle cells and fibrosis appeared in the myocardium. The pathogenesis of radiation pancarditis is thought to be dependent not only on the disturbance of microcirculation caused by endothelial cell damage of the capillaries, but also on alterations of the myocardial mitochondria as a result of direct injury.
通过对单次接受3000伦琴(I组)或300伦琴X射线照射(II组)的兔子进行1小时至6个月的观察,对辐射诱导的心脏损伤进行了形态学研究。I组和II组心脏病变没有本质区别。急性心外膜炎在照射后1小时就已发现,在1至2天时严重程度达到最高。在心肌中,出现心肌细胞变性和溶解、线粒体各种结构变化以及闰盘紊乱。间质组织中发生多形核细胞浸润和毛细血管内皮损伤。此外,常发现伴有或不伴有血栓形成的心内膜炎。II组心肌中的急性炎症比I组出现得晚,但消失得早。在后期,心外膜和心内膜最终发生纤维化。心肌中出现肌细胞糖蛋白变性和纤维化。辐射性全心炎的发病机制被认为不仅取决于毛细血管内皮细胞损伤引起的微循环紊乱,还取决于直接损伤导致的心肌线粒体改变。