Engler E, Matthias D, Becker C H
Exp Pathol (Jena). 1980;18(1):37-51. doi: 10.1016/s0014-4908(80)80070-6.
Autoradiographic, light and electron microscopic investigations on the effect of depot angiotensin on the hearts of rats suggested that the myocardium and the intramural vessels reacted with an activation of the mesenchymal and DNA metabolism already 3 hrs, after the injection of depot angiotensin. The reactions in the capillaries and small arterioles were dominating. Degenerative alterations could be found in the cardiac muscle cells only 9 hrs. after injection and culminated in infarction-like necroses and intensive mesenchymal proliferation after the 4th A II injection. Despite further daily applications of A II the degenerative and necrotic myocardial alterations will extensively diminish until the 14th day of experiment, while the mesenchymal activation and the enhanced DNA synthesis in the vessels remained unchanged. Thus an initial stage with the development of disseminated muscle fibre necroses and infarction-like alterations and a stage of compensatory adaptation may be distinguished in the heart after depot angiotensin injections.
对长效血管紧张素对大鼠心脏影响的放射自显影、光学和电子显微镜研究表明，在注射长效血管紧张素后3小时，心肌和壁内血管就因间充质和DNA代谢的激活而发生反应。毛细血管和小动脉中的反应最为明显。仅在注射后9小时，心肌细胞中就可发现退行性改变，并在第4次注射血管紧张素II后发展为梗死样坏死和强烈的间充质增殖。尽管此后每天继续注射血管紧张素II，但直到实验第14天，退行性和坏死性心肌改变将大幅减轻，而血管中的间充质激活和增强的DNA合成仍保持不变。因此，在注射长效血管紧张素后，心脏中可区分出一个以弥漫性肌纤维坏死和梗死样改变发展为特征的初始阶段和一个代偿性适应阶段。
