Role of nitric oxide in hepatic ischemia-reperfusion injury

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 IR...

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Veröffentlicht in:	World journal of gastroenterology : WJG 2010-12, Vol.16 (48), p.6079-6086
Hauptverfasser:	Siriussawakul, Arunotai, Zaky, Ahmed, Lang, John D
Format:	Artikel
Sprache:	eng
Schlagworte:	Humans Liver - blood supply Liver - cytology Liver - metabolism Liver - pathology Nitric Oxide - metabolism Nitric Oxide - therapeutic use Nitric Oxide Donors - metabolism Reperfusion Injury - drug therapy Reperfusion Injury - pathology Reperfusion Injury - physiopathology Topic Highlight
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Zusammenfassung:	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.
ISSN:	1007-9327 2219-2840
DOI:	10.3748/wjg.v16.i48.6079