• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Sustained exogenous administration of Met5-enkephalin protects against infarction in vivo.
【24h】

Sustained exogenous administration of Met5-enkephalin protects against infarction in vivo.

机译：持续外源性给予Met5-脑啡肽可预防体内梗塞。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The opioid antagonist naloxone abolishes infarct limitation by myocardial ischemic preconditioning, suggesting that one or more endogenous opioid peptides can mediate cardiac protection against ischemic damage. We tested the hypothesis that the naturally occurring opioid peptide Met5-enkephalin (ME) modulates myocardial infarct size in vivo. Experiments were conducted in barbiturate-anesthetized open-chest rabbits subjected to regional myocardial ischemia-reperfusion. ME was administered via osmotic minipump for 24 h. Infarct size was assessed with tetrazolium and is expressed as a percentage of the area at risk. Exogenous ME reduced the amount of the risk zone infarcted by approximately 60% compared with saline-treated controls. ME-induced protection was sensitive to opioid receptor blockade with naloxone [NAL 50 +/- 2% vs. ME + NAL 39 +/- 3%, P = not significant (NS)] and also to blockade of sarcolemmal and mitochondrial ATP-sensitive K+ (KATP) channels [5-hydroxydecanoate (5-HD) 33 +/- 3% vs. ME + 5-HD 43 +/- 8%, P = NS; and HMR-1098 60 +/- 3% vs. ME + HMR-1098 54 +/- 7%, P = NS]. We conclude that ME limits ischemic injury in vivo by an opioid receptor-mediated mechanism that involves both sarcolemmal and mitochondrial KATP channels.
机译：阿片样物质拮抗剂纳洛酮消除了心肌缺血预适应引起的梗塞局限性，表明一种或多种内源性阿片样物质肽可以介导针对缺血性损伤的心脏保护作用。我们测试了天然存在的阿片类肽Met5-脑啡肽（ME）调节体内心肌梗塞大小的假设。实验在巴比妥酸盐麻醉的开胸兔子进行局部心肌缺血-再灌注。通过渗透微型泵给予ME 24小时。用四唑鎓评估梗塞面积，并表示为危险区域的百分比。与生理盐水处理的对照组相比，外源性ME减少了梗死危险区的数量约60％。 ME诱导的保护对纳洛酮对阿片类药物受体的敏感[NAL 50 +/- 2％vs. ME + NAL 39 +/- 3％，P =不显着（NS）]，并且对肌膜和线粒体ATP-敏感的K +（KATP）通道[5-羟基癸酸酯（5-HD）33 +/- 3％，而ME + 5-HD 43 +/- 8％，P = NS;和HMR-1098 60 +/- 3％vs. ME + HMR-1098 54 +/- 7％，P = NS]。我们得出结论，ME通过阿片受体介导的机制（包括肌膜和线粒体KATP通道）来限制体内缺血性损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号