心肌缺血期间的膜磷脂代谢：过去、现在与未来
Membrane phospholipid metabolism during myocardial ischaemia: past, present and future.
作者信息
Sen A, Buja L M, Willerson J T, Chien K R
机构信息
Department of Internal Medicine, University of Texas Health Science Center, Dallas.
出版信息
Basic Res Cardiol. 1987;82 Suppl 1:121-5. doi: 10.1007/978-3-662-08390-1_15.
Alterations in myocardial membrane phospholipids may play an important role in the pathogenesis of ischaemic myocardial cell injury. Studies in canine myocardium, perfused rat heart, and cultured myocardial cells have demonstrated that the accumulation of free arachidonic acid correlates with the development of irreversible cell injury. Accumulation of other phospholipid hydrolysis products, including amphiphilic compounds such as lysophosphatidylcholine, has also been reported. The biochemical mechanisms which are responsible for phospholipid hydrolysis and arachidonic acid accumulation during ischaemia are unknown. This manuscript provides a synopsis of previous work in this field and suggests new directions for the field of myocardial phospholipid metabolism.
心肌膜磷脂的改变可能在缺血性心肌细胞损伤的发病机制中起重要作用。对犬心肌、灌注大鼠心脏和培养心肌细胞的研究表明，游离花生四烯酸的积累与不可逆细胞损伤的发展相关。也有报道称其他磷脂水解产物的积累，包括两亲性化合物如溶血磷脂酰胆碱。缺血期间负责磷脂水解和花生四烯酸积累的生化机制尚不清楚。本手稿概述了该领域以前的工作，并为心肌磷脂代谢领域提出了新的方向。
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