心肌缺血时磷脂改变与膜损伤。

K R Chien, J T Willerson, L M Buja
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引用次数: 4

摘要

几项独立研究表明,在心肌缺血期间膜磷脂存在降解。目前,大多数数据支持磷脂酶a的初始激活途径的磷脂降解。总磷脂降解的程度是每克湿重的纳摩尔量,与缺血性肝脏相反,在缺血性肝脏中,磷脂消耗的程度接近每克湿重的微摩尔水平。然而,体外研究表明,钙通透性和其他心肌细胞膜功能对纳米级磷脂降解很敏感。显然,在完整细胞和心脏制备中,需要进一步研究磷脂降解与ATP耗尽和缺氧时不可逆膜损伤的发展之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Phospholipid alterations and membrane injury during myocardial ischemia.

Several independent studies have demonstrated that there is a degradation of membrane phospholipids during myocardial ischemia. At present, most of the data support the initial activation of a phospholipase A pathway of phospholipid degradation. The extent of total phospholipid degradation is in the nanomole per gram wet weight quantity, as opposed to ischemic liver, in which the extent of phospholipid depletion approaches the micromole per gram wet weight level. However, in vitro studies suggest that calcium permeability properties and other myocardial cell membrane functions are sensitive to nanomole levels of phospholipid degradation. Clearly, further work is necessary in intact cell and heart preparations to correlate the degradation of phospholipid with the development of irreversible membrane injury during ATP depletion and hypoxia.

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