Suzuki K, Kawaharada U, Kobori K, Takatama M, Ooneda G, Fukuda T
Acta Pathol Jpn. 1986 Oct;36(10):1529-36. doi: 10.1111/j.1440-1827.1986.tb02824.x.
Electron microscopically the role of acid phosphatase (acid P) positive lysosomes in the pathogenesis of intramyocardial coronary artery lesions of hypertensive rats with bilaterally constricted renal arteries was studied. At 3 postoperative weeks, acid P positive lysosomes were increased in endothelial cells of the coronary arteries, but at 5 weeks and thereafter, they were decreased in number. In the intima, intimal smooth muscle cells with acid P positive lysosomes appeared at 3 postoperative weeks, but their number remained small as late as 9 postoperative weeks. The internal elastic lamina was fragmented into amorphous masses from 3 postoperative weeks, at 5 weeks and thereafter the fragmentation and disruption became severer, and at 9 weeks the lamina disappeared because of marked disruption. At 3 postoperative weeks, acid P positive extracellular lysosomes were observed in the gaps of the fragmented internal elastic lamina. At 5 weeks and thereafter, extracellular lysosomes and attenuated processes of medial smooth muscle cells with lysosomes were seen extending through the gaps of the fragmented internal elastic lamina. Necrosis of these extending cell processes and lysosomes remaining after the necrosis were observed. The findings suggested that the fragmentation and lytic change of the internal elastic lamina observed in hypertensive rat intramyocardial coronary arteries might be induced by extracellular lysosomes discharged not only from endothelial cells and intimal smooth muscle cells but also from the extending processes of medial smooth muscle cells into the gaps of the internal elastic lamina.
用电镜研究了双侧肾动脉狭窄的高血压大鼠心肌内冠状动脉病变发病机制中酸性磷酸酶（酸性P）阳性溶酶体的作用。术后3周，冠状动脉内皮细胞中酸性P阳性溶酶体增多，但在5周及之后，其数量减少。在内膜，术后3周出现含酸性P阳性溶酶体的内膜平滑肌细胞，但其数量在术后9周时仍较少。术后3周内弹性膜开始断裂成无定形团块，5周及之后断裂和破坏变得更严重，9周时弹性膜因明显破坏而消失。术后3周，在断裂的内弹性膜间隙中观察到酸性P阳性细胞外溶酶体。5周及之后，可见细胞外溶酶体和含溶酶体的中膜平滑肌细胞的延长突起穿过断裂的内弹性膜间隙。观察到这些延长的细胞突起坏死以及坏死后残留的溶酶体。这些发现提示，高血压大鼠心肌内冠状动脉中观察到的内弹性膜的断裂和溶解变化可能是由不仅从内皮细胞和内膜平滑肌细胞，而且从中膜平滑肌细胞的延长突起释放到内弹性膜间隙中的细胞外溶酶体所诱导的。
