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抗氧化储备的相对不足可能导致心力衰竭。

A relative deficit in antioxidant reserve may contribute in cardiac failure.

作者信息

Singal P K, Kirshenbaum L A

机构信息

Cardiovascular Sciences Division, St Boniface General Hospital Research Centre, Winnipeg, Manitoba.

出版信息

Can J Cardiol. 1990 Mar;6(2):47-9.

PMID:2138050
Abstract

Antioxidant enzyme activities, including superoxide dismutase, glutathione peroxidase and catalase, are known to be altered under various physiological and pathophysiological conditions. There is a significant increase in some of these activities in the myocardium during stable hyperfunctional heart hypertrophy subsequent to pressure overload, as well as after exercise training in rats. Hearts with increased antioxidant capacity have been reported to be more resistant to in vivo and in vitro oxidative stress. On the other hand, cardiomyopathy and heart failure under a variety of conditions are accompanied by increased free radicals and lipid peroxidation. These data lead to the hypothesis that maintained or improved function during compensated heart hypertrophy may be supported by an increased antioxidant capacity, and a relative deficit in this 'antioxidant reserve' may contribute in the decompensated state.

摘要

抗氧化酶活性,包括超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶,已知在各种生理和病理生理条件下会发生改变。在压力超负荷后稳定的高功能心脏肥大期间,以及在大鼠运动训练后,心肌中的某些此类活性会显著增加。据报道,抗氧化能力增强的心脏对体内和体外氧化应激更具抵抗力。另一方面,在各种情况下的心肌病和心力衰竭都伴随着自由基增加和脂质过氧化。这些数据导致这样一种假设,即代偿性心脏肥大期间维持或改善的功能可能由增加的抗氧化能力支持,而这种“抗氧化储备”的相对不足可能导致失代偿状态。

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