在豚鼠和大鼠中，酒精摄入通过物种特异性信号传导减少缺血再灌注损伤。

Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats.

作者信息

Miyamae M, Camacho S A, Zhou H Z, Diamond I, Figueredo V M

机构信息

Department of Medicine (Cardiology), San Francisco General Hospital, University of California, San Francisco, California 94110, USA.

出版信息

Am J Physiol. 1998 Jul;275(1):H50-6. doi: 10.1152/ajpheart.1998.275.1.H50.

DOI:10.1152/ajpheart.1998.275.1.H50

PMID:9688895

Abstract

We recently discovered that regular alcohol consumption reduces ischemia-reperfusion injury to the same degree as ischemic preconditioning in guinea pig hearts. Ischemic preconditioning, like this cardioprotective effect of alcohol, is mediated by adenosine signaling in guinea pigs. In rats, ischemic preconditioning may be mediated predominantly by alpha1-adrenergic signaling. To be certain that this protective effect of alcohol is a general biological response, we searched for alcohol's cardioprotection in rat and identified a potential signaling mechanism. Hearts isolated from alcohol-fed guinea pigs and rats were subjected to ischemia-reperfusion. Hearts from alcohol-fed animals showed greater recovery of left ventricular developed pressure than controls (guinea pigs, 46 vs. 29%; rats, 50 vs. 31%) and decreased myocyte necrosis assessed by creatine kinase release (guinea pigs, 204 +/- 42 vs. 440 +/- 70 U . ml-1 . g dry wt-1; rats 158 +/- 13 vs. 328 +/- 31 U . ml-1 . g dry wt-1). Adenosine receptor blockade [8-(p-sulfophenyl)theophylline] abolished alcohol's protection in guinea pig but not rat hearts. By contrast, alpha1-adrenergic blockade (prazosin) abolished alcohol's protection in rat but not guinea pig hearts. We conclude that regular alcohol consumption reduces ischemia-reperfusion injury and is mediated by species-specific signaling mechanisms. A major goal of cardiovascular research is to find a pharmacologically induced chronic state of preconditioning. Understanding the mechanisms of alcohol's cardioprotection against ischemia-reperfusion injury may aid in reaching this goal.

摘要

我们最近发现，在豚鼠心脏中，规律饮酒对缺血再灌注损伤的减轻程度与缺血预处理相同。与酒精的这种心脏保护作用一样，豚鼠的缺血预处理是由腺苷信号介导的。在大鼠中，缺血预处理可能主要由α1-肾上腺素能信号介导。为确定酒精的这种保护作用是否为一种普遍的生物学反应，我们在大鼠中探寻酒精的心脏保护作用并确定了一种潜在的信号传导机制。将从喂食酒精的豚鼠和大鼠分离出的心脏进行缺血再灌注处理。喂食酒精动物的心脏左心室舒张末压恢复程度高于对照组（豚鼠，46% 对 29%；大鼠，50% 对 31%），并且通过肌酸激酶释放评估的心肌细胞坏死减少（豚鼠，204±42 对 440±70 U·ml-1·g 干重-1；大鼠，158±13 对 328±31 U·ml-1·g 干重-1）。腺苷受体阻断剂[8-(对磺基苯基)茶碱]消除了酒精对豚鼠心脏的保护作用，但对大鼠心脏无效。相比之下，α1-肾上腺素能阻断剂（哌唑嗪）消除了酒精对大鼠心脏的保护作用，但对豚鼠心脏无效。我们得出结论，规律饮酒可减轻缺血再灌注损伤，且由物种特异性信号传导机制介导。心血管研究的一个主要目标是找到一种通过药理学诱导的慢性预处理状态。了解酒精对缺血再灌注损伤的心脏保护机制可能有助于实现这一目标。