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腺苷和一氧化氮疗法减轻手术缺血再灌注损伤

Reduction in surgical ischemic-reperfusion injury with adenosine and nitric oxide therapy.

作者信息

Vinten-Johansen J, Zhao Z Q, Sato H

机构信息

Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1096, USA.

出版信息

Ann Thorac Surg. 1995 Sep;60(3):852-7. doi: 10.1016/0003-4975(95)00571-2.

DOI:10.1016/0003-4975(95)00571-2
PMID:7677546
Abstract

Ischemia and reperfusion impair the inherent capacity of the heart to protect itself from related pathophysiologic events by reducing endogenous oxygen radical scavengers and inhibitors. However, other endogenously produced agents, notably adenosine and nitric oxide, are produced during ischemia, reperfusion, or both. These autacoids have several cardioprotection actions in common, particularly antineutrophil effects and inhibition of endothelial-neutrophil interactions, which are key initial steps in ischemic-reperfusion injury. Studies have shown that nitric oxide exerts cardioprotection primarily during reperfusion. Adenosine, on the other hand, protects the myocardium to some extent during both ischemia and reperfusion, thereby covering both periods during which myocardial injury may be sustained during a cardiac operation. Native adenosine or active analogues, or donors of nitric oxide, may be given before or in conjunction with cardioplegia solutions. However, these endogenous agents can also be pharmacologically recruited to provide a new potent therapeutic approach against surgical ischemic-reperfusion injury. This article reviews the cardioprotective effects of primarily endogenous nitric oxide and adenosine in both nonsurgical and surgical models of ischemia-reperfusion injury. Both adenosine and nitric oxide provide potent cardioprotection in surgical and nonsurgical models of ischemia-reperfusion. An important mechanism in this cardioprotection is attenuation of neutrophil-mediated damage.

摘要

缺血再灌注通过减少内源性氧自由基清除剂和抑制剂,损害心脏保护自身免受相关病理生理事件影响的固有能力。然而,在缺血、再灌注或两者过程中会产生其他内源性物质,尤其是腺苷和一氧化氮。这些自分泌物质具有一些共同的心脏保护作用,特别是抗中性粒细胞作用以及抑制内皮细胞与中性粒细胞的相互作用,而这是缺血再灌注损伤关键的起始步骤。研究表明,一氧化氮主要在再灌注期间发挥心脏保护作用。另一方面,腺苷在缺血和再灌注期间均能在一定程度上保护心肌,从而涵盖了心脏手术期间心肌可能持续受损的两个阶段。天然腺苷或活性类似物,或一氧化氮供体,可在心脏停搏液给药前或与之联合使用。然而,这些内源性物质也可通过药理学方法加以利用,以提供一种针对手术缺血再灌注损伤的新的有效治疗方法。本文综述了主要内源性一氧化氮和腺苷在非手术和手术缺血再灌注损伤模型中的心脏保护作用。腺苷和一氧化氮在手术和非手术缺血再灌注模型中均具有强大的心脏保护作用。这种心脏保护作用的一个重要机制是减轻中性粒细胞介导的损伤。

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