Short- and long-term influence of beta-adrenergic antagonists after acute myocardial infarction.

Short- and long-term influence of beta-adrenergic antagonists after acute myocardial infarction.
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急性心肌梗死后β-肾上腺素能拮抗剂的短期和长期影响。

DOI:
10.1016/s0002-9149(84)80307-0
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发表时间:
1984
期刊:
The American journal of cardiology
影响因子:
--
通讯作者:
Buja,LM
Buja,LM
中科院分区:
--
文献类型:
--
作者:
Willerson,JT;Buja,LM

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在冠状动脉闭塞后,在细胞损伤逐渐变得更严重的演变期,左心室中的储存库释放出儿茶酚胺,受损的心肌细胞暴露于相对高浓度的儿茶酚胺。此外,在实验动物模型中,永久性冠状动脉闭塞1小时内β-肾上腺素能受体密度显著增加,亲和力无任何改变。最近的数据表明,在实验动物模型中,冠状动脉闭塞后30至60分钟内α-肾上腺素能受体密度增加。与实验动物心脏中正常灌注的组织相比,在发展性心肌损伤的早期阶段给予儿茶酚胺可导致严重损伤的肾上腺素能生化反应升高。因此,有充分的理由预期β-肾上腺素能拮抗剂将保护缺血性心肌,并可能降低进展性急性心肌梗死(AMI)个体中危及生命的心律失常的发生率。动物模型研究表明,在冠状动脉闭塞后最初几分钟内给予β-肾上腺素能拮抗剂可降低心肌坏死的最终程度。本文综述了几项不同试验的临床资料,这些试验中使用β-肾上腺素能受体拮抗剂(1)保护缺血心肌和保存心室功能,(2)降低AMI患者严重室性心律失常的严重程度。本文介绍了AMI后患者长期使用β-肾上腺素能拮抗剂在延长生命和降低再梗死风险方面的作用。
After coronary arterial occlusion, catecholamines are released from storage depots in the left ventricle and injured myocardial cells are exposed to relatively high concentrations of catecholamines during the evolutionary period in which cell injury is becoming progressively more severe. In addition, in experimental animal models, there is a substantial increase in β-adrenergic receptor density without any alteration in affinity within 1 hour of permanent coronary arterial occlusion. Recent data suggest that α-adrenergic receptor density increases within 30 to 60 minutes after coronary arterial occlusion in experimental animal models. The administration of catecholamines during the early phases of evolving myocardial injury can result in heightened adrenergic biochemical responses in severely injured compared with normally perfused tissue in the hearts of experimental animals. Thus, there is adequate rationale for anticipating that β-adrenergic antagonists would protect ischemic myocardium and potentially reduce the incidence of life-threatening arrhythmias in individuals with evolving acute myocardial infarction (AMI). Studies in animal models demonstrate that the administration of β-adrenergic antagonists in the first few minutes after coronary artery occlusion may reduce the ultimate extent of myocardial necrosis. Clinical data from several different trials in which β-adrenergic antagonists were administered to (1) protect ischemic myocardium and preserve ventricular function and (2) reduce the severity of serious ventricular arrhythmias in patients with AMI are reviewed. The effects of longer-term administration of β-adrenergic antagonists in patients after AMI in prolonging life and reducing risk of reinfarction are presented.
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