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全脑缺血和再灌注对人体心肌影响的超微结构评估

Ultrastructural evaluation of the effects of global ischemia and reperfusion on human myocardium.

作者信息

Schaper J, Schwarz F, Kittstein H, Kreisel E, Winkler B, Hehrlein F W

出版信息

Thorac Cardiovasc Surg. 1980 Oct;28(5):337-42. doi: 10.1055/s-2007-1022104.

Abstract

During open-heart surgery, myocardial biopsies were taken from 31 patients undergoing aortic valve replacement on total cardiopulmonary bypass. The first needle biopsy was taken before the induction of cardiac arrest (Kirsch cardioplegia), the second at the end of global ischemia, and the third during the reperfusion period. The tissue was investigated by electron microscopy using a semiquantitative scoring system for changes in both myocytes and blood vessels. Mitochondrial volume and surface density were determined by morphometry. Reversible ischemic injury of moderate to severe degree occurred in cardiac cells and in small blood vessels. On reperfusion, signs of damage regressed earlier in myocardial than in vascular tissue. Morphometry revealed significant mitochondrial swelling during the reperfusion phase, but this was not present after ischemia alone. It is concluded that Kirsch cardioplegia as applied here, is unable to protect the heart from ischemic cellular damage.

摘要

在心脏直视手术中,从31例接受全心肺转流主动脉瓣置换术的患者身上获取心肌活检样本。第一次针吸活检在心脏停搏诱导前(Kirsch心脏停搏液)进行,第二次在全心缺血结束时进行,第三次在再灌注期进行。使用半定量评分系统对心肌细胞和血管的变化进行电子显微镜检查。通过形态计量学确定线粒体体积和表面密度。心脏细胞和小血管出现中度至重度可逆性缺血损伤。再灌注时,心肌损伤迹象比血管组织消退得更早。形态计量学显示再灌注期线粒体明显肿胀,但仅缺血后未出现这种情况。结论是,此处应用的Kirsch心脏停搏液无法保护心脏免受缺血性细胞损伤。

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