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氧自由基介导的心肌和血管功能障碍。

O2 free radical-mediated myocardial and vascular dysfunction.

作者信息

Jackson C V, Mickelson J K, Pope T K, Rao P S, Lucchesi B R

出版信息

Am J Physiol. 1986 Dec;251(6 Pt 2):H1225-31. doi: 10.1152/ajpheart.1986.251.6.H1225.

DOI:10.1152/ajpheart.1986.251.6.H1225
PMID:3789177
Abstract

In the present investigation electrolysis of a physiological buffer solution for 2 min with a constant current (20 mA, DC stainless steel anode) was observed to generate free radicals, determined by a luminol assay. Rabbit isolated hearts perfused with physiological buffer subjected to electrolysis were observed to undergo an increase in coronary artery perfusion pressure (PP) and in left ventricular end-diastolic pressure (LVEDP), 80 +/- 4 and 52 +/- 7 mmHg, respectively. Immediately after electrolysis of the physiological buffer, the hearts were observed to accumulate and retain (8-fold) more 125I-labeled albumin than hearts perfused with normal buffer without electrolysis, indicating an increased vascular permeability. The free radical scavengers, dimethyl sulfoxide (DMSO) and catalase (CAT), provided significant protection of the hearts against the changes in PP, LVEDP, and vascular permeability. This study demonstrates that toxic oxygen species generated independently of circulating blood elements or enzymatic reactions can have a direct effect on the vasculature of an isolated heart leading to alterations in cardiac function. The protection afforded by the addition of DMSO or CAT to the perfusion system would suggest that the OH. radical and H2O2 were the reactive oxygen species involved in producing the observed vascular and cardiac effects.

摘要

在本研究中,观察到用恒流(20 mA,直流不锈钢阳极)对生理缓冲溶液进行2分钟电解会产生自由基,这是通过鲁米诺测定法确定的。观察到用经过电解的生理缓冲液灌注的兔离体心脏,其冠状动脉灌注压(PP)和左心室舒张末期压力(LVEDP)分别升高,达到80±4 mmHg和52±7 mmHg。在生理缓冲液电解后立即观察到,与用未电解的正常缓冲液灌注的心脏相比,这些心脏积累并保留(8倍)了更多的125I标记白蛋白,这表明血管通透性增加。自由基清除剂二甲亚砜(DMSO)和过氧化氢酶(CAT)为心脏提供了显著保护,使其免受PP、LVEDP和血管通透性变化的影响。本研究表明,独立于循环血液成分或酶促反应产生的有毒氧物种可直接影响离体心脏的血管系统,导致心脏功能改变。向灌注系统中添加DMSO或CAT所提供的保护表明,OH·自由基和H2O2是参与产生观察到的血管和心脏效应的活性氧物种。

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