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[大鼠体内缺血再灌注心肌中氧自由基的产生]

[Oxygen free radical generation in ischemic-reperfused myocardium of rat in vivo].

作者信息

Huang N

出版信息

Zhonghua Yi Xue Za Zhi. 1990 Dec;70(12):691-3, 48.

PMID:1963374
Abstract

Many studies have provided indirect evidence that there is a relationship between oxygen free radical and myocardial ischemic-reperfusion injury. In this study, we applied ESR spectroscopy to measure oxygen free radical generation in the acutely ischemic-reperfused heart of rat in vivo. The experimental model was established by 45 min ligation of the left anterior descending coronary artery (LAD) and 10 min reperfusion in vivo. The myocardial samples taken for ESR measurement were fresh-freezing tissue pieces. Meanwhile, the tissue ultrastructure was observed. We also observed the protective effect of superoxide dismutase (SOD) on myocardial ischemic-reperfusion injury. The results showed: 1. Large amounts of oxygen free radical were generated in the course of postischemic reperfusion. The amount of oxygen free radical produced in this process was positively related to the extent of myocardial damage. Oxygen free radical was at least one of the major cause of rat myocardial reperfusion injury observed in this experiment. 2. SOD could scavenge oxygen free radical and prevent or reduce reperfusion injury of rat heart in vivo.

摘要

许多研究已提供间接证据表明氧自由基与心肌缺血-再灌注损伤之间存在关联。在本研究中,我们应用电子自旋共振光谱法来测量大鼠急性缺血-再灌注心脏在体内产生的氧自由基。通过在体内结扎左冠状动脉前降支(LAD)45分钟并再灌注10分钟来建立实验模型。用于电子自旋共振测量的心肌样本是新鲜冷冻的组织块。同时,观察组织超微结构。我们还观察了超氧化物歧化酶(SOD)对心肌缺血-再灌注损伤的保护作用。结果显示:1. 缺血后再灌注过程中产生大量氧自由基。此过程中产生的氧自由基量与心肌损伤程度呈正相关。氧自由基至少是本实验中观察到的大鼠心肌再灌注损伤的主要原因之一。2. SOD可清除氧自由基并预防或减轻大鼠心脏在体内的再灌注损伤。

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