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内源性阿片肽在心脏保护中的作用。

The Role of Endogenous Opioids in Cardioprotection.

机构信息

Department of Cardiac Surgery and Transplantation, University Hospital Nancy-Brabois, Nancy, France.

出版信息

Adv Neurobiol. 2024;35:381-395. doi: 10.1007/978-3-031-45493-6_19.

DOI:10.1007/978-3-031-45493-6_19
PMID:38874733
Abstract

The opioid system involves opioid receptors (OPRs) and endogenous opioid peptides.This chapter will focus on the distribution of OPRs in the cardiovascular system, the expression pattern in the heart, the activation by opioid peptides, and the effects of OPRs activation with potential relevance in cardiovascular performance. In the heart, OPRs are co-expressed with beta adrenergic receptors (β-ARs) in the G-protein-coupled receptor (GPCR) superfamily, functionally cross-talk with β-Ars and modify catecholamine-induced effects. They are involved in cardiac contractility, energy metabolism, myocyte survival or death, vascular resistance. The effects of the opioid system in the regulation of systemic circulation at both the central and peripheral level are presented. The pathways are discussed under physiological (i.e., aging) and pathological conditions (atherosclerosis, heart failure, essential hypertension, ischemic stress). Stimulation of OPRs not only inhibits cardiac excitation-contraction coupling, but also protects the heart against hypoxic and ischemic injury. An enhanced sensitivity to opioids of endocrine organs and neuronal systems is operative in hypertensive patients. The opioid system can be pharmacologically engaged to selectively mimic these responses via cardiac and nervous signaling. The clinical opportunities for the use of cardioprotective effects of opioids require future investigations to provide more specific details of the impact on cardiac performance and electrophysiological properties.

摘要

阿片样物质系统涉及阿片受体(OPRs)和内源性阿片肽。本章将重点介绍 OPR 在心血管系统中的分布、在心脏中的表达模式、阿片肽的激活作用,以及 OPR 激活对心血管功能的潜在影响。在心脏中,OPRs 与β肾上腺素能受体(β-ARs)共同表达于 G 蛋白偶联受体(GPCR)超家族中,与β-ARs 功能相互作用,并调节儿茶酚胺诱导的作用。它们参与心肌收缩力、能量代谢、心肌存活或死亡、血管阻力的调节。本文介绍了阿片样物质系统在调节全身循环方面的中枢和外周水平的作用。讨论了在生理(如衰老)和病理条件(动脉粥样硬化、心力衰竭、原发性高血压、缺血应激)下的途径。OPR 的刺激不仅抑制心脏兴奋-收缩偶联,而且还保护心脏免受缺氧和缺血损伤。在高血压患者中,内分泌器官和神经元系统对阿片类药物的敏感性增强。阿片样物质系统可以通过心脏和神经信号来进行药理学干预,以选择性模拟这些反应。需要进一步研究阿片类药物的心脏保护作用的临床应用机会,以提供对心脏功能和电生理特性影响的更具体细节。

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本文引用的文献

1
Prospects for Creation of Cardioprotective and Antiarrhythmic Drugs Based on Opioid Receptor Agonists.基于阿片受体激动剂的心脏保护和抗心律失常药物的研发前景
Med Res Rev. 2016 Sep;36(5):871-923. doi: 10.1002/med.21395. Epub 2016 May 16.
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Opioid receptors and cardioprotection - 'opioidergic conditioning' of the heart.阿片受体与心脏保护——心脏的“阿片能预处理”
Br J Pharmacol. 2015 Apr;172(8):2026-50. doi: 10.1111/bph.13042. Epub 2015 Feb 27.
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Role of central and peripheral opioid receptors in the cardioprotection of intravenous morphine preconditioning.
中枢和外周阿片受体在静脉注射吗啡预处理中的心脏保护作用。
Ir J Med Sci. 2011 Dec;180(4):881-5. doi: 10.1007/s11845-011-0734-0. Epub 2011 Jul 29.
4
Opioid Peptide gene expression in the myocardial cell.心肌细胞中阿片肽基因的表达。
Trends Cardiovasc Med. 1998 Apr;8(3):102-10. doi: 10.1016/S1050-1738(97)00140-0.
5
Comparative analysis of the cardioprotective properties of opioid receptor agonists in a rat model of myocardial infarction.比较分析阿片受体激动剂在大鼠心肌梗死模型中心脏保护作用。
Acad Emerg Med. 2010 Nov;17(11):1239-46. doi: 10.1111/j.1553-2712.2010.00910.x.
6
U50,488H postconditioning reduces apoptosis after myocardial ischemia and reperfusion.U50,488H 后处理减少心肌缺血再灌注后的细胞凋亡。
Life Sci. 2011 Jan 3;88(1-2):31-8. doi: 10.1016/j.lfs.2010.10.018. Epub 2010 Oct 27.
7
Activation of kappa-opioid receptors at reperfusion affords cardioprotection in both rat and mouse hearts.再灌注时κ-阿片受体的激活对大鼠和小鼠心脏均具有心脏保护作用。
Basic Res Cardiol. 2008 Sep;103(5):454-63. doi: 10.1007/s00395-008-0726-z. Epub 2008 May 23.
8
Effects of beta-endorphin on endothelial/monocytic endothelin-1 and nitric oxide release mediated by mu1-opioid receptors: a potential link between stress and endothelial dysfunction?β-内啡肽对由μ1阿片受体介导的内皮细胞/单核细胞内皮素-1释放及一氧化氮释放的影响:应激与内皮功能障碍之间的潜在联系?
Endothelium. 2007 Mar-Apr;14(2):65-71. doi: 10.1080/10623320701346585.
9
GSK3beta inhibition and K(ATP) channel opening mediate acute opioid-induced cardioprotection at reperfusion.糖原合成酶激酶3β抑制和ATP敏感性钾通道开放介导急性阿片类药物在再灌注时诱导的心脏保护作用。
Basic Res Cardiol. 2007 Jul;102(4):341-9. doi: 10.1007/s00395-007-0651-6. Epub 2007 Apr 23.
10
Mediating delta-opioid-initiated heart protection via the beta2-adrenergic receptor: role of the intrinsic cardiac adrenergic cell.通过β2-肾上腺素能受体介导δ-阿片类药物引发的心脏保护作用:心脏内源性肾上腺素能细胞的作用
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