Department of Anesthesiology and Pain Medicine and the VA Puget Sound Healthcare System, the University of Washington School of Medicine, Seattle, WA 98108, United States.
World J Gastroenterol. 2010 Dec 28;16(48):6079-86. doi: 10.3748/wjg.v16.i48.6079.
Hepatic ischemia-reperfusion injury (IRI) occurs upon restoration of hepatic blood flow after a period of ischemia. Decreased endogenous nitric oxide (NO) production resulting in capillary luminal narrowing is central in the pathogenesis of IRI. Exogenous NO has emerged as a potential therapy for IRI based on its role in decreasing oxidative stress, cytokine release, leukocyte endothelial-adhesion and hepatic apoptosis. This review will highlight the influence of endogenous NO on hepatic IRI, role of inhaled NO in ameliorating IRI, modes of delivery, donor drugs and potential side effects of exogenous NO.
肝脏缺血再灌注损伤（IRI）发生于肝脏缺血一段时间后血流恢复时。内源性一氧化氮（NO）生成减少导致毛细血管管腔变窄，这在 IRI 的发病机制中起核心作用。基于其在降低氧化应激、细胞因子释放、白细胞内皮黏附及肝凋亡中的作用，外源性 NO 已成为治疗 IRI 的一种潜在疗法。本文将重点阐述内源性 NO 对肝脏 IRI 的影响、吸入性 NO 改善 IRI 的作用、NO 的传递方式、供体药物及外源性 NO 的潜在副作用。
