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促红细胞生成素模拟缺血预处理。

Erythropoietin mimics ischemic preconditioning.

作者信息

Baker John E

机构信息

Pharmacology and Toxicology, Biochemistry and Pediatric Surgery, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

出版信息

Vascul Pharmacol. 2005 Apr-May;42(5-6):233-41. doi: 10.1016/j.vph.2005.02.004. Epub 2005 Mar 17.

Abstract

Ischemic preconditioning is a powerful endogenous phenomenon in which brief periods of a sub-toxic ischemic insult induce robust protection against future, lengthy, lethal ischemia. The cardioprotective effects of ischemic preconditioning are manifest in all species studied so far, including humans. The ability to reproduce the cardioprotective effects of ischemic preconditioning with pharmacological agents raises the possibility that a drug may ultimately be introduced into clinical practice to treat human hearts undergoing ischemia/reperfusion. This chapter focuses on erythropoietin (Epo), a drug that has already been approved for humans and is in current use for the treatment of anemia associated with chronic renal failure, HIV infection, cancer patients on chemotherapy, and to reduce allogenic blood transfusion in surgery patients. Several recent studies have suggested that this cytokine possesses properties far beyond its capacity to produce red blood cells such as the ability to protect tissues including brain, kidney and heart against injury caused by ischemia/reperfusion. Cardioprotection conferred by Epo has been shown to be equal in magnitude to that conferred by ischemic preconditioning. However, the underlying mechanisms by which Epo protects the heart against injury caused by ischemia remain unknown.

摘要

缺血预处理是一种强大的内源性现象,即短暂的亚毒性缺血损伤可诱导对未来长时间致死性缺血的强大保护作用。缺血预处理的心脏保护作用在迄今研究的所有物种中都有体现,包括人类。用药物复制缺血预处理的心脏保护作用的能力增加了这样一种可能性,即最终可能会有一种药物被引入临床实践,用于治疗经历缺血/再灌注的人类心脏。本章重点介绍促红细胞生成素(Epo),这是一种已被批准用于人类的药物,目前用于治疗与慢性肾衰竭、HIV感染、接受化疗的癌症患者相关的贫血,以及减少手术患者的异体输血。最近的几项研究表明,这种细胞因子具有远远超出其产生红细胞能力的特性,例如能够保护包括脑、肾和心脏在内的组织免受缺血/再灌注损伤。Epo赋予的心脏保护作用已被证明在程度上与缺血预处理赋予的保护作用相当。然而,Epo保护心脏免受缺血损伤的潜在机制仍然未知。

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