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腺苷A1类似物与缺血预处理对离体兔心脏的不同作用。

Different effects of an adenosine A1 analogue and ischemic preconditioning in isolated rabbit hearts.

作者信息

Lasley R D, Noble M A, Konyn P J, Mentzer R M

机构信息

Department of Surgery, University of Wisconsin School of Medicine, Madison 53792-0001, USA.

出版信息

Ann Thorac Surg. 1995 Dec;60(6):1698-703. doi: 10.1016/0003-4975(95)00717-2.

Abstract

BACKGROUND

Ischemic preconditioning reduces infarct size, but its effects on postischemic function are variable. Adenosine, which is thought to play a role in ischemic preconditioning, reduces both infarct size and postischemic dysfunction. The purpose of this study was to compare the cardioprotective effects of ischemic preconditioning and an adenosine A1 receptor agonist on recovery of function and infarct size in isolated rabbit hearts.

METHODS

Krebs buffer-perfused hearts (at least 7 per group) were subjected to 60 minutes of global ischemia (37 degrees C) and 60 minutes of reperfusion. Ventricular function was assessed by measuring left ventricular developed pressure, and infarct size (percentage of the left ventricle) was determined by tetrazolium staining.

RESULTS

Control hearts exhibited 34% +/- 6% infarct size and 56% +/- 4% recovery of preischemic left ventricular developed pressure. Ischemic preconditioning reduced infarct size to 13% +/- 1% but had no effect on recovery of function (65% +/- 5%). Hearts treated with the adenosine A1 agonist R-phenylisopropyladenosine for 5 minutes immediately before ischemia exhibited both reduced infarct size (10% +/- 2%) and enhanced postischemic recovery of left ventricular developed pressure (86% +/- 3%). Termination of the R-phenylisopropyladenosine treatment before ischemia eliminated its beneficial effects. The adenosine A1 receptor antagonist DPCPX blocked both of the effects of R-phenylisopropyladenosine but did not block ischemic preconditioning.

CONCLUSIONS

These results demonstrate fundamental differences between the cardioprotective effects of adenosine A1 receptor activation and ischemic preconditioning.

摘要

背景

缺血预处理可减小梗死面积,但其对缺血后心功能的影响并不一致。腺苷被认为在缺血预处理中发挥作用,它既能减小梗死面积,又能减轻缺血后功能障碍。本研究旨在比较缺血预处理与腺苷A1受体激动剂对离体兔心功能恢复和梗死面积的心脏保护作用。

方法

用Krebs缓冲液灌注心脏(每组至少7个),使其经历60分钟全心缺血(37℃)和60分钟再灌注。通过测量左心室舒张末压评估心室功能,并用四氮唑染色法测定梗死面积(左心室的百分比)。

结果

对照心脏的梗死面积为34%±6%,缺血前左心室舒张末压恢复率为56%±4%。缺血预处理使梗死面积减小至13%±1%,但对功能恢复无影响(65%±5%)。在缺血前立即用腺苷A1激动剂R-苯异丙基腺苷处理心脏5分钟,可使梗死面积减小(10%±2%),并增强缺血后左心室舒张末压的恢复(86%±3%)。在缺血前终止R-苯异丙基腺苷处理会消除其有益作用。腺苷A1受体拮抗剂DPCPX可阻断R-苯异丙基腺苷的两种作用,但不阻断缺血预处理。

结论

这些结果表明腺苷A1受体激活和缺血预处理的心脏保护作用存在根本差异。

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