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肌膜磷脂脂肪酸组成与通透性

Sarcolemmal phospholipid fatty acid composition and permeability.

作者信息

Bester R, Lochner A

机构信息

Department of Medical Physiology and Biochemistry, University of Stellenbosch Medical School, Tygerberg (Republic of South Africa).

出版信息

Biochim Biophys Acta. 1988 Jun 22;941(2):176-86. doi: 10.1016/0005-2736(88)90178-2.

DOI:10.1016/0005-2736(88)90178-2
PMID:3382645
Abstract

In this study, the mechanism of ischaemia-induced increased sarcolemmal permeability, as manifested by release of intracellular enzymes, was investigated. The role of changes in the sarcolemmal phospholipid bilayer in this process was evaluated by experimental modulation of the phospholipid fatty acid composition. The isolated perfused rat heart subjected to low-flow hypoxia, was used as a model of global ischaemia. Glucose as well as saturated (palmitate) and unsaturated (linoleate) long-chain fatty acids were used as substrates. Hearts perfused with palmitate or linoleate (1.5 mM, fatty acid/albumin ratio, 3.4) showed a significantly higher rate of lactate dehydrogenase release in both control and ischaemic conditions than hearts perfused with glucose (10 mM). Lactate dehydrogenase release in the fatty acid-perfused hearts was associated with a significant increase in the percentage unsaturation of the sarcolemmal phospholipid fatty acids. Glucose-perfused hearts, on the other hand, showed only minor changes in the sarcolemmal phospholipid fatty acid composition. Attempts to correlate enzyme release directly with an increase in the percentage unsaturation of phospholipid fatty acids failed, since enzyme release was also stimulated in control fatty-acid-perfused hearts which (when compared with glucose) contained a higher percentage saturated phospholipid fatty acids. The results suggest that myocardial ischaemia, apart from changes in the sarcolemmal phospholipid fatty acid composition, also induces several other changes in sarcolemmal composition (e.g., cholesterol loss) which may affect is permeability for macromolecules.

摘要

在本研究中,对缺血诱导的肌膜通透性增加(表现为细胞内酶释放)的机制进行了研究。通过对磷脂脂肪酸组成进行实验性调节,评估了肌膜磷脂双分子层变化在此过程中的作用。将经历低流量缺氧的离体灌注大鼠心脏用作整体缺血模型。葡萄糖以及饱和(棕榈酸)和不饱和(亚油酸)长链脂肪酸用作底物。与灌注葡萄糖(10 mM)的心脏相比,灌注棕榈酸或亚油酸(1.5 mM,脂肪酸/白蛋白比率为3.4)的心脏在对照和缺血条件下乳酸脱氢酶释放率均显著更高。脂肪酸灌注心脏中乳酸脱氢酶的释放与肌膜磷脂脂肪酸不饱和度百分比的显著增加相关。另一方面,葡萄糖灌注心脏的肌膜磷脂脂肪酸组成仅出现微小变化。由于在对照脂肪酸灌注心脏(与葡萄糖相比,其饱和磷脂脂肪酸百分比更高)中酶释放也受到刺激,因此未能将酶释放与磷脂脂肪酸不饱和度百分比的增加直接关联起来。结果表明,心肌缺血除了引起肌膜磷脂脂肪酸组成变化外,还会诱导肌膜组成的其他几种变化(例如胆固醇丢失),这可能会影响其对大分子的通透性。

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