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顿抑心肌的线粒体NADH氧化酶和ATP酶活性增强。

Stunned myocardium has increased mitochondrial NADH oxidase and ATPase activities.

作者信息

Vandeplassche G, Hermans C, Thoné F, Borgers M

机构信息

Department of Life Sciences, Janssen Research Foundation, Beerse, Belgium.

出版信息

Cardioscience. 1991 Mar;2(1):47-53.

PMID:1832316
Abstract

Ten anesthetized, open-chest dogs were subjected to occlusion of the left anterior descending coronary artery for 15 minutes, followed by reperfusion for 150 minutes. Hemodynamics were recorded and regional myocardial contraction was measured sonometrically. The hearts were then fixed in situ using glutaraldehyde for cytochemical studies. Systolic wall thickening remained unchanged in the non-ischemic myocardium, but was significantly depressed (stunned) in the area of the left anterior descending coronary artery during reperfusion. NADH oxidase and ATPase activities were very weakly present in mitochondria from non-ischemic myocardium. In the ischemic endocardium, irreversibly injured cells had mitochondria which were severely altered and contained no reaction products to the two enzymes. In contrast, high NADH oxidase and ATPase activities were present in mitochondria from the less severely injured cells of the endocardial zone of stunned areas. Since this zone is particularly susceptible to ischemia in dogs, the high mitochondrial NADH oxidase and ATPase activities may be early signs of ischemic damage, reflecting a disturbance in mitochondrial respiratory activity in stunned myocardium.

摘要

十只麻醉开胸犬接受左冠状动脉前降支闭塞15分钟,随后再灌注150分钟。记录血流动力学,并通过超声心动图测量局部心肌收缩情况。然后用戊二醛原位固定心脏用于细胞化学研究。非缺血心肌的收缩期室壁增厚保持不变,但在再灌注期间左冠状动脉前降支区域显著降低(顿抑)。非缺血心肌线粒体中NADH氧化酶和ATP酶活性非常弱。在缺血的心内膜中,不可逆损伤细胞的线粒体严重改变,对这两种酶无反应产物。相比之下,顿抑区心内膜带损伤较轻细胞的线粒体中存在高NADH氧化酶和ATP酶活性。由于该区域在犬中特别易受缺血影响,线粒体高NADH氧化酶和ATP酶活性可能是缺血损伤的早期迹象,反映了顿抑心肌线粒体呼吸活动的紊乱。

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