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首页> 外文期刊>Bulletin of experimental biology and medicine >Role of beta-Adrenoceptors and L-Type Ca2+-Channels in the Mechanism of Reperfusion-Induced Heart Injury
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Role of beta-Adrenoceptors and L-Type Ca2+-Channels in the Mechanism of Reperfusion-Induced Heart Injury

机译:β肾上腺素能受体和L型Ca2 +通道在再灌注引起的心脏损伤机制中的作用

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摘要

We studied the effects of beta-adrenoceptor antagonists propranolol and nadolol and L-type Ca2+-channel blocker verapamil on cardiac reperfusion injury developed after 45-min coronary occlusion. The substances were injected intravenously 5 min before reperfusion. The results indicate that activation of beta-adrenoceptors and opening of L-type Ca2+-channels promote the development of cardiac reperfusion injury, while blockage of beta-adrenoceptors and/or L-type Ca2+-channels prevents reoxygenation-induced myocardial injury. Propranolol, nadolol, and verapamil can produce infraction-limiting effects after onset of ischemic heart injury.
机译:我们研究了β-肾上腺素能受体拮抗剂普萘洛尔和那多洛尔以及L型Ca2 +通道阻滞剂维拉帕米对冠状动脉闭塞45分钟后发生的心脏再灌注损伤的影响。在再灌注前5分钟静脉内注射该物质。结果表明,β-肾上腺素受体的激活和L型Ca2 +通道的开放促进了心脏再灌注损伤的发展,而β-肾上腺素受体和/或L型Ca2 +-通道的阻滞阻止了复氧引起的心肌损伤。普萘洛尔,纳多洛尔和维拉帕米可在缺血性心脏损伤发作后产生违规限制作用。

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