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缺血缺氧状态下的心肌收缩功能

Myocardial contractile function during ischemia and hypoxia.

作者信息

Allen D G, Orchard C H

出版信息

Circ Res. 1987 Feb;60(2):153-68. doi: 10.1161/01.res.60.2.153.

Abstract

There is good evidence that elevated [Ca2+]i, produced by an influx of Ca2+ in exchange for Na+, is the underlying pathology in reperfusion or reoxygenation damage. Further measurements of [Na+]i and [Ca2+]i during ischemia and reperfusion, coupled with information about metabolic levels, are needed to confirm or refute this hypothesis. Contributions to cell damage by other mechanisms, e.g., oxygen free radicals, certainly cannot yet be excluded.

摘要

有充分证据表明,由Ca2+内流以交换Na+所产生的细胞内钙离子浓度升高,是再灌注或复氧损伤的潜在病理机制。需要在缺血和再灌注期间进一步测量细胞内钠离子浓度和钙离子浓度,并结合代谢水平的信息,以证实或反驳这一假说。当然,其他机制(如氧自由基)对细胞损伤的作用尚未能排除。

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