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脓毒性休克对大鼠肺组织中磷脂酰胆碱重塑机制的影响。

Influence of septic shock upon phosphatidylcholine remodeling mechanism in rat lung.

作者信息

von Wichert P, Temmesfeld M, Meyer W

出版信息

Biochim Biophys Acta. 1981 Jun 23;664(3):487-97. doi: 10.1016/0005-2760(81)90127-2.

DOI:10.1016/0005-2760(81)90127-2
PMID:6791696
Abstract

Septic shock in rats lead to pulmonary disorders associated with alterations of phospholipid metabolism. The ratio between phosphatidylcholine and lysophosphatidylcholine is lowered both in lung tissue and in pulmonary surfactant because enzymes of phosphatidylcholine remodeling mechanism are distinctly affected by septic shock. Specific activity of phospholipase A2 is enhanced 5-fold while specific activities of lysolecithin acyltransferase and lysolecithin : lysolecithin acyltransferase are only slightly increased or remain unchanged. Beyond that, palmitic acid content of lung tissue phosphatidylcholine is significantly reduced and replaced mainly by arachidonic acid. The release of this fatty acid by action of phospholipase A2 may lead via intermediates to the generation of potent mediators such as prostaglandins, thromboxane or slow-reacting substance.

摘要

大鼠脓毒症休克会导致与磷脂代谢改变相关的肺部疾病。肺组织和肺表面活性物质中磷脂酰胆碱与溶血磷脂酰胆碱的比例均降低,因为磷脂酰胆碱重塑机制的酶受到脓毒症休克的显著影响。磷脂酶A2的比活性提高了5倍,而溶血卵磷脂酰基转移酶和溶血卵磷脂:溶血卵磷脂酰基转移酶的比活性仅略有增加或保持不变。除此之外,肺组织磷脂酰胆碱的棕榈酸含量显著降低,主要被花生四烯酸取代。磷脂酶A2作用释放的这种脂肪酸可能通过中间产物导致产生强效介质,如前列腺素、血栓素或慢反应物质。

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引用本文的文献

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Mechanism responsible for endotoxin-induced lung microsomal dysfunction in rats.大鼠内毒素诱导肺微粒体功能障碍的机制。
Lung. 1983;161(6):361-8. doi: 10.1007/BF02713885.
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In vivo inhibition of phospholipase A2 in rat lung by an beta-adrenergic agonist.β-肾上腺素能激动剂对大鼠肺中磷脂酶A2的体内抑制作用。
Agents Actions. 1983 Apr;13(2-3):233-4. doi: 10.1007/BF01967339.
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A phospholipase inhibitor modifies the pulmonary damage associated with peritonitis in rabbits.一种磷脂酶抑制剂可改善兔腹膜炎相关的肺损伤。
Intensive Care Med. 1987;13(4):284-90. doi: 10.1007/BF00265119.
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