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氧自由基的损伤程度决定制动应激对损伤心脏心室电稳定性的影响

卞劲松, 王幼林, 李德兴

南京医科大学药理教研室. 江苏, 南京 210029

摘要

该文比较了在制动应激过程中正常及阿霉素心肌损伤大鼠心室电稳定性(VES)的变化间的差异。应激各时程，ivgtt乌头碱(0.8μg/min)，心肌损伤大鼠出现心律失常的潜伏期均较正常鼠明显缩短，说明其较正常大鼠更易发生心律失常。正常大鼠随应激时程的延长，VES的变化表现为先降后升，而阿霉素大鼠制动2h，室速、室颤潜伏期及其持续时间虽也显著缩短，但制动8h心律失常发生却无明显改变，提示持续制动应激对正常心肌VES的升高作用在损伤心肌中消失。由于阿霉素大鼠制动2h，心率及心肌组织cAMP含量无显著变化，而8h时却显著下降，说明与正常心脏不同，损伤心脏VES在持续制动应激过程中的变化并非主要取决于交感神经的活性。制动2h，损伤心肌SOD活性下降，MDA含量升高，制动8h两者均无明显改变。因此，应激所致损伤心肌VES的改变主要与心肌组织氧自由基的损伤程度有密切关系。

关键词： 固定术; 应激; 心律失常; 阿霉素; 乌头碱; 自由基类

Immobilization stress induced changes of ventricular electric stability in damaged heart depends on the extent of free radical damage

Bian Jinsong, Wang Youlin, Li Dexing

Department of Pharmacology, Nanjing Medical University. Nanjing 210029, Jiangsu, China

Abstract

Following persistent irnmobilization stress, differences in changes of ventricular electric stability (VES) between normal (Nor) rats and rats with myocardial damage induced by doxorubicin (Dox) were studied and compared. The latencies of arrhythmias due to iwtt aconitine (at a rate of 0.8 #mu#g/min) were significantly shorter in Dox rats than in Nor rats, ie, it was easier for Dox rats to develop axrhythmias. Persistent immobilization stress caused an initial decrease followed by a subsequent increase of VES in Nor rats. However, Dox rats following a 8 h' stress show no significant changes in latency and duration of arrhythmias, in contrast with the shortening of the two indexes in rats only immobilized for 2 h, indicating that the increased VES induced by prolonged stress in Nor rats was eliminated by Dox. Both heart rate and cAMP content in myocAnial tissue of Dox rats show no obvious changes in 2 h' stress, but significantly decreased in 8h' immobilizati0n rats.

Key words: Immobilization;Stress;Arrhythmia;Doxorubicin;aconitine;Free radicals

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引用本文：

卞劲松, 王幼林, 李德兴. 氧自由基的损伤程度决定制动应激对损伤心脏心室电稳定性的影响 [J]. 生理学报 1997; 49 (5): .

Bian Jinsong, Wang Youlin, Li Dexing. Immobilization stress induced changes of ventricular electric stability in damaged heart depends on the extent of free radical damage. Acta Physiol Sin 1997; 49 (5): (in Chinese with English abstract).