Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats.
Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats.
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饮酒通过豚鼠和大鼠的物种特异性信号传导减少缺血再灌注损伤。
DOI：
10.1152/ajpheart.1998.275.1.h50
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Figueredo,VM
中科院分区：
文献类型：
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作者：
Miyamae,M;Camacho,SA;Zhou,HZ;Diamond,I;Figueredo,VM
我们最近发现，定期饮酒减少缺血再灌注损伤的程度与豚鼠心脏缺血预处理相同。缺血预处理，像酒精的心脏保护作用一样，是由腺苷信号在豚鼠体内介导的。在大鼠中，缺血预适应可能主要由α1-肾上腺素能信号介导。为了确定酒精的这种保护作用是一种普遍的生物学反应，我们在大鼠中寻找酒精的心脏保护作用，并确定了一种潜在的信号机制。从酒精喂养的豚鼠和大鼠分离的心脏进行缺血再灌注。与对照组相比，来自酒精喂养动物的心脏显示出更大的左心室发展压力恢复（豚鼠，46 vs. 29%;大鼠，50 vs. 31%）和通过肌酸激酶释放评估的肌细胞坏死减少（豚鼠，204 ± 42 vs. 440 ± 70 U·ml-1·g干重-1;大鼠，158 ± 13 vs. 328 ± 31 U·ml-1·g干重-1）。腺苷受体阻断剂[8-（对磺基苯基）茶碱]可阻断酒精对豚鼠心脏的保护作用，但对大鼠心脏无影响。相比之下，α1-肾上腺素能阻滞剂（哌唑嗪）在大鼠而不是豚鼠心脏中消除了酒精的保护作用。我们的结论是，定期饮酒减少缺血再灌注损伤，是由物种特异性信号传导机制介导的。心血管研究的一个主要目标是寻找一种由心脏刺激引起的慢性预适应状态。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。
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 α1-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, α1-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.