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冠状动脉手术后的心肌和微血管损伤及其通过再灌注方式的减轻。

Myocardial and microvascular injury following coronary surgery and its attenuation by mode of reperfusion.

作者信息

Lindal S, Gunnes S, Lund I, Straume B K, Jørgensen L, Sørlie D

机构信息

Department of Pathology, University Hospital of Tromsø, Norway.

出版信息

Eur J Cardiothorac Surg. 1995;9(2):83-9. doi: 10.1016/s1010-7940(05)80024-7.

Abstract

In 14 patients undergoing coronary surgery, repeated atrial biopsies were obtained before and at the end of ischemia, and at 20 and 60 min of reperfusion. In half of the patients reperfusion was initiated with an abrupt rise in blood temperature and pressure, in the other half with a gradual rise. The biopsies were prepared for transmission electron microscopy and analyzed by stereological technique. In all biopsies, myocytic injury, as revealed by mitochondrial changes and intracellular edema, occurred following ischemia (P = 0.0003 and 0.007, respectively). The intracellular edema regressed following 20 min of reperfusion (P = 0.008). The myocytic mitochondrial changes persisted during reperfusion towards the end of the observation period (P = 0.0001). Interstitial edema increased following ischemia (P = 0.007) and persisted following 60 min of reperfusion (P = 0.009). The capillary part was significantly reduced after 20 min of reperfusion (P = 0.003), probably reflecting interstitial edema. Most changes were reversible in nature, although foci of irreversible changes were shown. In patients with a gradual start of reperfusion there was a significant regression of interstitial edema (P = 0.005) at 60 min reperfusion compared to the patients with an abrupt start, where the same changes seemed to persist or even increase. The study demonstrates that "reperfusion injury" occurs in human myocardium. It can be discerned from "ischemic" injury, and it may be reduced by a gentle mode of reperfusion.

摘要

在14例接受冠状动脉手术的患者中,于缺血前、缺血结束时以及再灌注20分钟和60分钟时重复进行心房活检。一半患者再灌注开始时血液温度和压力急剧升高,另一半患者则是逐渐升高。活检组织经处理用于透射电子显微镜检查,并采用体视学技术进行分析。在所有活检组织中,缺血后均出现了以线粒体变化和细胞内水肿为特征的心肌细胞损伤(分别为P = 0.0003和0.007)。再灌注20分钟后细胞内水肿消退(P = 0.008)。心肌细胞线粒体变化在再灌注期间持续至观察期末(P = 0.0001)。缺血后间质水肿增加(P = 0.007),再灌注60分钟后仍持续存在(P = 0.009)。再灌注20分钟后毛细血管部分显著减少(P = 0.003),这可能反映了间质水肿。尽管出现了不可逆变化的病灶,但大多数变化本质上是可逆的。与再灌注开始时急剧升高的患者相比,再灌注开始时逐渐升高的患者在再灌注60分钟时间质水肿有显著消退(P = 0.005),而后者相同的变化似乎持续存在甚至加重。该研究表明“再灌注损伤”发生在人体心肌中。它可与“缺血性”损伤相鉴别,并且通过温和的再灌注方式可能会减轻。

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