摘要
背景:阻塞血管的早期再灌注对恢复血液流向缺血心肌来挽救心肌组织和改善临床结果至关重要。然而,一段时间的缺血后,这种再灌注策略可能引起称为心肌再灌注损伤的进一步的心肌损伤。再灌注损伤的表现包括心律失常,心肌梗塞和微血管功能障碍,以及明显的心肌细胞死亡。建议过度生成活性氧,细胞内钙超载和炎性细胞浸润是心肌缺血再灌注损伤的最重要特征。 目的:讨论了针对线粒体通透性转换孔的治疗心肌再灌注损伤的各种药理学干预措施,包括抗氧化黄酮醇,硫化氢,腺苷,阿片样物质,肠降血糖素基治疗和环孢菌素A。 结论:参与再灌注损伤的过程可能为改善心肌梗死后结局提供指标,但到目前为止,临床上尚未达到目的。
关键词: 心脏保护,缺血再灌注,抗氧化剂,活性氧,黄酮醇,硫化氢,腺苷,阿片样物质,肠降血糖素基治疗,环孢菌素A.
图形摘要
Current Drug Targets
Title:New Pharmacological Approaches to the Prevention of Myocardial Ischemia- Reperfusion Injury
Volume: 18 Issue: 15
关键词: 心脏保护,缺血再灌注,抗氧化剂,活性氧,黄酮醇,硫化氢,腺苷,阿片样物质,肠降血糖素基治疗,环孢菌素A.
摘要: Background: Early reperfusion of the blocked vessel is critical to restore the blood flow to the ischemic myocardium to salvage myocardial tissue and improve clinical outcome. This reperfusion strategy after a period of ischemia, however, may elicit further myocardial damage named myocardial reperfusion injury. The manifestations of reperfusion injury include arrhythmias, myocardial stunning and micro-vascular dysfunction, in addition to significant cardiomyocyte death. It is suggested that an overproduction of reactive oxygen species, intracellular calcium overload and inflammatory cell infiltration are the most important features of myocardial ischemia-reperfusion injury.
Objective: In this review, various pharmacological interventions to treat myocardial reperfusion injury including the antioxidant flavonols, hydrogen sulfide, adenosine, opioids, incretin-based therapies and cyclosporin A which targets the mitochondrial permeability transition pore are discussed.
Conclusion: The processes involved in reperfusion injury might provide targets for improved outcomes after myocardial infarction but thus far that aim has not been met in the clinic.
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Cite this article as:
New Pharmacological Approaches to the Prevention of Myocardial Ischemia- Reperfusion Injury, Current Drug Targets 2017; 18 (15) . https://dx.doi.org/10.2174/1389450116666151001112020
DOI https://dx.doi.org/10.2174/1389450116666151001112020 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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