2007
Decreased intrahepatic response to α1‐adrenergic agonists in lipopolysaccharide‐treated rats is located in the sinusoidal area and depends on Kupffer cell function
Lee C, Loureiro‐Silva M, Abraldes JG, Iwakiri Y, Haq O, Groszmann RJ. Decreased intrahepatic response to α1‐adrenergic agonists in lipopolysaccharide‐treated rats is located in the sinusoidal area and depends on Kupffer cell function. Journal Of Gastroenterology And Hepatology 2007, 22: 893-900. PMID: 17498219, DOI: 10.1111/j.1440-1746.2007.04922.x.Peer-Reviewed Original ResearchConceptsLipopolysaccharide-treated ratsKupffer cell functionVascular responsesAdrenergic agonistsKupffer cellsNormal liverSinusoidal areaNitric oxide synthase inhibitorCell functionOxide synthase inhibitorRole of KupfferVascular tone controlNitric oxide overproductionKrebs-Henseleit solutionNitric oxide productionΑ1-adrenergic agonistDose-response curveIntrahepatic responseMicrovascular abnormalitiesSecond doseEndotoxemic ratsLiver perfusionSynthase inhibitorMethoxamineGadolinium chloride
2003
A liver-specific nitric oxide donor improves the intra-hepatic vascular response to both portal blood flow increase and methoxamine in cirrhotic rats
Loureiro-Silva MR, Cadelina GW, Iwakiri Y, Groszmann RJ. A liver-specific nitric oxide donor improves the intra-hepatic vascular response to both portal blood flow increase and methoxamine in cirrhotic rats. Journal Of Hepatology 2003, 39: 940-946. PMID: 14642609, DOI: 10.1016/j.jhep.2003.09.018.Peer-Reviewed Original ResearchConceptsBlood flow increasesCirrhotic ratsPortal pressureUrsodeoxycholic acidLiver perfusionFlow/pressure curvesNO donorAscitic cirrhotic ratsBlood volume expansionBasal heart rateSitu liver perfusionNitric oxide productionNitric oxide donorDose/response curveBlood flow measurementsPortal hypertensionHemodynamic effectsArterial pressureFlow increasesVascular responsesControl ratsBlood infusionBACKGROUND/Heart rateOxide donor
2002
Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension
Iwakiri Y, Tsai MH, McCabe TJ, Gratton JP, Fulton D, Groszmann RJ, Sessa WC. Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension. AJP Heart And Circulatory Physiology 2002, 282: h2084-h2090. PMID: 12003815, DOI: 10.1152/ajpheart.00675.2001.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic alpha-1 Receptor AgonistsAndrostadienesAnimalsEnzyme InhibitorsHypertension, PortalLigationMaleMesenteric Artery, SuperiorMethoxamineNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIOmega-N-MethylargininePhosphorylationPortal VeinProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyVasoconstrictor AgentsWortmanninConceptsEndothelial nitric oxide synthasePortal vein ligationPhosphorylation of eNOSMesenteric arterial bedPortal hypertensionPVL groupArterial bedNO productionMale Sprague-Dawley ratsEarly portal hypertensionMonomethyl-L-arginineNitric oxide synthaseSprague-Dawley ratsExcessive NO productionG protein-coupled receptorsVivo perfusion studiesPVL ratsProtein-coupled receptorsPerfusion pressureSham groupVein ligationENOS expressionOxide synthaseReduced responsivenessKinase/Akt pathway