Chien K R, Willerson J T, Buja L M
Adv Myocardiol. 1985;5:347-53. doi: 10.1007/978-1-4757-1287-2_26.
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.
多项独立研究表明,心肌缺血期间存在膜磷脂降解。目前,大多数数据支持磷脂降解的磷脂酶A途径的初始激活。总磷脂降解程度为每克湿重纳摩尔量,这与缺血肝脏不同,在缺血肝脏中磷脂消耗程度接近每克湿重微摩尔水平。然而,体外研究表明,钙通透性特性和其他心肌细胞膜功能对纳摩尔水平的磷脂降解敏感。显然,在完整细胞和心脏制剂中进行进一步研究,以将磷脂降解与ATP耗竭和缺氧期间不可逆膜损伤的发展联系起来是必要的。