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[缺血后时期脂质过氧化与心肌收缩功能取决于心脏低温保护水平]

[Lipid peroxidation and myocardial contractile function in the post-ischemic period depending on the level of hypothermic protection of the heart].

作者信息

Boiarinov G A, Kontorshchikova K N, Mukhina I V

出版信息

Biull Eksp Biol Med. 1991 Oct;112(10):374-6.

PMID:1804347
Abstract

The experiments on rats isolated hearts showed lipid peroxidation state to depend on myocardial cooling level in ischemic period. Cooling to 8-12 degrees C does not induce significant impairment in the system of lipid peroxidation/antioxidant activity, thus preventing the development of reperfusion impairment in cardiac activity restoration. Temperature decrease to 4-6 degrees C during the ischemic period results in lipid peroxidation, antioxidant cell system exhaustion and impairment of contractive myocardial function in reperfusion.

摘要

对大鼠离体心脏进行的实验表明,脂质过氧化状态取决于缺血期心肌的冷却程度。冷却至8 - 12摄氏度不会对脂质过氧化/抗氧化活性系统造成显著损害,从而预防心脏活动恢复过程中再灌注损伤的发生。缺血期温度降至4 - 6摄氏度会导致脂质过氧化、抗氧化细胞系统耗竭以及再灌注时心肌收缩功能受损。

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