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World J Gastroenterol. Dec 28, 2010; 16(48): 6079-6086
Published online Dec 28, 2010. doi: 10.3748/wjg.v16.i48.6079
Published online Dec 28, 2010. doi: 10.3748/wjg.v16.i48.6079
Role of nitric oxide in hepatic ischemia-reperfusion injury
Arunotai Siriussawakul, Ahmed Zaky, John D Lang, 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
Author contributions: Siriussawakul A, Zaky A and Lang JD all significantly contributed to the content of this paper.
Correspondence to: John D Lang, MD, Associate Professor, 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. jdlang@u.washington.edu
Telephone: +1-206-7642854 Fax: +1-206-7642914
Received: June 28, 2010
Revised: September 7, 2010
Accepted: September 14, 2010
Published online: December 28, 2010
Revised: September 7, 2010
Accepted: September 14, 2010
Published online: December 28, 2010
Abstract
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.
Keywords: Nitric oxide; Liver; Ischemia-reperfusion injury; Drug delivery