Tanno F, Akiyama K, Geshi E, Yanagishita T, Konno N, Katagiri T
Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
Jpn Circ J. 1992 Sep;56(9):911-20. doi: 10.1253/jcj.56.911.
Impairment of sarcolemmal permeability after the initiation of acute ischemic myocardial injury was studied using an ionic lanthanum (La3+) probe in electron microscopy. Acute ischemic myocardium was induced by ligation of the left anterior descending coronary artery in dogs. In normal cardiac myocytes La is localized exclusively in the extracellular space. i.e. on the glycocalyx, in the T-system and in intercalated discs, with normal fine structures. In ischemic myocardial cells, La deposits were found in the cytosolic space in 22% of subendocardial cells with mild to moderate, but non-necrotic, fine structural changes as early as 30 min. The number of myocytes with La deposition increased with advancing ischemic injury, and necrotic fine structural changes were recognized following ischemia for 60 min. These results indicate that deposition of La occurs before the appearance of irreversible morphologic alterations in ischemic myocardial cells, and suggest an increased permeability of the sarcolemma for Ca2+ and the development of degradation of plasma membrane integrity.
利用离子镧(La3+)探针,通过电子显微镜研究急性缺血性心肌损伤发生后肌膜通透性的损害情况。通过结扎犬左冠状动脉前降支诱导急性缺血性心肌。在正常心肌细胞中,镧仅定位于细胞外间隙,即位于糖萼、T小管和闰盘中,且结构正常。在缺血心肌细胞中,早在30分钟时,就在22%的内膜下细胞的胞质空间中发现了镧沉积,这些细胞具有轻度至中度但非坏死性的细微结构变化。随着缺血损伤的进展,有镧沉积的心肌细胞数量增加,缺血60分钟后可识别出坏死性细微结构变化。这些结果表明,镧沉积发生在缺血心肌细胞出现不可逆形态改变之前,并提示肌膜对Ca2+的通透性增加以及质膜完整性遭到破坏。