缺血后处理、ATP后处理减轻兔缺血再灌注损伤:与腺苷受体激活有关

被引：5

作者：

刘方 ^{[1
]}

廉哲勋 ^{[1
]}

王永彬 ^{[2
]}

葛毅萍 ^{[3
]}

机构：

[1] 青岛大学医学院附属医院心内科

[2] 青岛大学医学院附属医院急诊科

[3] 青岛大学医学院

来源：

现代生物医学进展 | 2007年 / 03期

关键词：

缺血再灌注损伤; 缺血后处理; 腺苷受体;

D O I：

10.13241/j.cnki.pmb.2007.03.011

中图分类号：

R363 [病理生理学];

学科分类号：

100104 ;

摘要：

目的:近期实验研究显示,在再灌注的早期给予短暂、重复的缺血再灌(缺血后处理Postconditioning)能够减轻心肌再灌注损伤。本实验旨在探明三磷酸腺苷(ATP)用于缺血后处理是否产生上述保护效应,以及了解腺苷受体在此保护作用机制中的地位。方法:家兔开胸后左前降支均给予40min结扎和180min的再灌注,并随机分为5组:(1)对照组;(2)缺血后处理组;(3)ATP后处理组;(4)缺血后处理+SPT(硫苯茶碱)组;(5)SPT对照组。于实验终点测定心肌梗死面积(TTC染色),血浆CK-MB、SOD、MDA含量。结果:和时照组相比,缺血后处理组与ATP后处理组心梗面积减少(p<0．05),CK-MB也显著降低(p<O．05)。在SPT+后处理组,SPT消除了缺血后处理的上述减少心梗面积作用(p<0．05)。此外,在两个后处理组MDA含量明显降低(p<0．05),SOD含量明显升高(p<0．05),同样地,在SPT+后处理组发现SPT取消了缺血后处理的减轻再灌注损伤作用。结论:ATP后处理具有与机械后处理相同的减轻心肌缺血再灌注损伤作用,而SPT消除缺血后处理保护作用的现象提示,该保护作用的机制可能与腺苷受体的激活有关。

引用

页码：353 / 355

页数：3

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