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缺血和心脏停搏后氨基酸对线粒体和心脏功能的保护作用。

Protection of mitochondrial and heart function by amino acids after ischemia and cardioplegia.

作者信息

Shug A L, Madsen D, Dobbie R, Paulson D J

机构信息

Department of Neurology, University of Wisconsin, Madison.

出版信息

Life Sci. 1994;54(8):567-77. doi: 10.1016/0024-3205(94)90008-6.

Abstract

The effects of amino acids in protecting against ischemic/reperfusion injury were tested in two experimental models: the isolated perfused rat heart subjected to 21 min of zero flow ischemia (37 degrees) followed by 40 min of reperfusion and the isolated perfused rabbit heart subjected to 300 min of cardioplegic arrest (29 degrees) followed by 60 min of reperfusion. In both cases, the addition of amino acids to the perfusion medium significantly improved the recovery of cardiac contractile function. The protective effects of amino acids were associated with a preservation of mitochondrial respiratory activity. These findings suggest that amino acids by replenishing mitochondrial matrix levels of critical TCA cycle substrates, such as malate, stimulate mitochondrial respiration and thereby enhance the recovery of heart function.

摘要

在两个实验模型中测试了氨基酸对缺血/再灌注损伤的保护作用:对离体灌注大鼠心脏进行21分钟的零流量缺血(37摄氏度),随后进行40分钟的再灌注;对离体灌注兔心脏进行300分钟的心脏停搏(29摄氏度),随后进行60分钟的再灌注。在这两种情况下,向灌注培养基中添加氨基酸均显著改善了心脏收缩功能的恢复。氨基酸的保护作用与线粒体呼吸活性的保留有关。这些发现表明,氨基酸通过补充三羧酸循环关键底物(如苹果酸)的线粒体基质水平,刺激线粒体呼吸,从而增强心脏功能的恢复。

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