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内毒素和血小板活化因子对大鼠心脏脂质氧化的影响。

Effect of endotoxin and platelet-activating factor on lipid oxidation in the rat heart.

作者信息

Wang X, Evans R D

机构信息

Nuffield Department of Anaesthetics, University of Oxford, Radcliffe Infirmary, Woodstock Road, Oxford, OX2 6HE, UK.

出版信息

J Mol Cell Cardiol. 1997 Jul;29(7):1915-26. doi: 10.1006/jmcc.1997.0430.

DOI:10.1006/jmcc.1997.0430
PMID:9236145
Abstract

The effects of endotoxin and platelet-activating factor (PAF) administered in vivo and in vitro on lipid oxidation by isolated perfused working rat heart were investigated and compared. Endotoxin administered in vivo decreased oleate oxidation in perfused hearts and caused increased accumulation of lipid in myocardial tissue; this was accompanied by a dose-dependent inhibition of cardiac mechanical function. There was no effect on triolein (chylomicron) oxidation. By contrast, PAF administered in vivo caused a small (non-significant) increase in the oxidation rate of oleate and triolein, and also increased myocardial lipoprotein lipase activity. Cardiac mechanical function was not inhibited by PAF-indeed pretreatment of animals by PAF administered in vivo protected the heart from the decline in function associated with subsequent fatty acid perfusion. Administration of endotoxin during perfusion in vitro did not affect oleate or triolein oxidation and cardiac mechanical function was unchanged; PAF administered in vitro caused an early increase in oleate oxidation and a later increase in triolein oxidation. Administration of both endotoxin and PAF in vitro increased myocardial lipoprotein lipase activity. PAF is unlikely to be responsible for all of the effects of endotoxin on cardiac lipid metabolism.

摘要

研究并比较了体内和体外给予内毒素和血小板活化因子(PAF)对离体灌注的正常工作大鼠心脏脂质氧化的影响。体内给予内毒素可降低灌注心脏中油酸的氧化,并导致心肌组织中脂质积累增加;这伴随着对心脏机械功能的剂量依赖性抑制。对三油酸甘油酯(乳糜微粒)氧化没有影响。相比之下,体内给予PAF可使油酸和三油酸甘油酯的氧化速率有小幅(无统计学意义)增加,并且还增加了心肌脂蛋白脂肪酶活性。PAF并未抑制心脏机械功能——实际上,体内给予PAF对动物进行预处理可保护心脏免受随后脂肪酸灌注所导致的功能下降的影响。体外灌注期间给予内毒素不影响油酸或三油酸甘油酯的氧化,心脏机械功能未改变;体外给予PAF可使油酸氧化早期增加,三油酸甘油酯氧化后期增加。体外同时给予内毒素和PAF可增加心肌脂蛋白脂肪酶活性。PAF不太可能是内毒素对心脏脂质代谢所有作用的原因。

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