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代偿性左心室肥厚时心外膜动脉和心内膜下小动脉中内皮G蛋白偶联受体途径的改变。

Alterations in the endothelial G-protein coupled receptor pathway in epicardial arteries and subendocardial arterioles in compensated left ventricular hypertrophy.

作者信息

Aubin Marie-Claude, Gendron Marie-Eve, Lebel Vickie, Thorin Eric, Tardif Jean-Claude, Carrier Michel, Perrault Louis P

机构信息

Research Center, Montreal Heart Institute and Université de Montréal, Montreal (QC), Canada.

出版信息

Basic Res Cardiol. 2007 Mar;102(2):144-53. doi: 10.1007/s00395-006-0626-z. Epub 2006 Sep 29.

Abstract

The present study was designed to compare alterations of endothelium-dependent vasorelaxation in coronary epicardial arteries and subendocardial arterioles occurring in left ventricular hypertrophy (LVH) secondary to 60 days of aortic banding in a porcine model. Development of LVH was documented by echocardiogram and the endothelial function of subendocardial and epicardial vessels was studied by constructing concentration-response curves in a pressure myograph and standard organ chambers, respectively. 5-HT induced relaxations were reduced (p<0.05) in both vessel types isolated from pigs with LVH. Dilations of subendocardial arterioles and epicardial vessels to UK14304 were depressed by LVH. In the presence of Nomega-nitro-L-arginine (L-NNA), EDHF solely accounts for BK-induced relaxations; it fully compensates for the loss of NO in arterioles, but only partially in epicardial arteries isolated from LVH swine. Endothelium-independent relaxations induced by SNP were not altered in both vessel types from the LVH group. In a porcine model of LVH secondary to 60 days of aortic banding, the associated coronary endothelial dysfunction preferentially involves Gi-protein mediated relaxations in arterioles and arteries but also affects Gq-protein mediated relaxations in epicardial coronary arteries.

摘要

本研究旨在比较猪模型中,主动脉缩窄60天继发左心室肥厚(LVH)时,冠状动脉心外膜动脉和心内膜下小动脉中内皮依赖性血管舒张的变化。通过超声心动图记录LVH的发展,并分别在压力肌动描记器和标准器官腔室中构建浓度-反应曲线,研究心内膜下和心外膜血管的内皮功能。从患有LVH的猪分离的两种血管类型中,5-羟色胺诱导的舒张均降低(p<0.05)。LVH抑制了心内膜下小动脉和心外膜血管对UK14304的舒张作用。在存在Nω-硝基-L-精氨酸(L-NNA)的情况下,内皮衍生超极化因子单独介导BK诱导的舒张;它完全补偿了小动脉中一氧化氮的损失,但仅部分补偿了从LVH猪分离的心外膜动脉中一氧化氮的损失。LVH组的两种血管类型中,硝普钠诱导的非内皮依赖性舒张均未改变。在主动脉缩窄60天继发LVH的猪模型中,相关的冠状动脉内皮功能障碍优先涉及小动脉和动脉中Gi蛋白介导的舒张,但也影响心外膜冠状动脉中Gq蛋白介导的舒张。

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