Bacterial translocation in cirrhotic rats stimulates eNOS-derived NO production and impairs mesenteric vascular contractility
Wiest R, Das S, Cadelina G, Garcia-Tsao G, Milstien S, Groszmann R. Bacterial translocation in cirrhotic rats stimulates eNOS-derived NO production and impairs mesenteric vascular contractility. Journal Of Clinical Investigation 1999, 104: 1223-1233. PMID: 10545521, PMCID: PMC409820, DOI: 10.1172/jci7458.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacterial TranslocationDose-Response Relationship, DrugLiver Cirrhosis, ExperimentalLymph NodesMaleMesenteric ArteriesMethoxamineNitric OxideNitric Oxide SynthasePerfusionPressureProtein IsoformsRatsRats, Sprague-DawleyStress, MechanicalTumor Necrosis Factor-alphaVasoconstrictionVasoconstrictor AgentsConceptsMesenteric lymph nodesEndothelial NO synthaseTNF-alpha productionAscitic cirrhotic ratsBacterial translocationCirrhotic ratsMesenteric vasculatureNitric oxidePresence of BTSuperior mesenteric arterial bedMesenteric arterial bedNitro-L-arginineTNF-alpha synthesisVascular hyporesponsivenessArterial vasodilationLiver cirrhosisLymph nodesVascular contractilityVascular responsesTNF-alphaArterial bedNO inhibitorNOS activityNO overproductionNO synthase