Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats.docVIP

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Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats.doc

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Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats

Gansteretal.CriticalCare2010,14:R165 /content/14/5/R165 RESEARCH OpenAccess Effectsofhydrogensulfideonhemodynamics, inflammatoryresponseandoxidativestress duringresuscitatedhemorrhagicshockinrats FrédériqueGanster1,2,6,MélanieBurban1,MathildedelaBourdonnaye1,LionelFizanne1,OlivierDouay1, LaurentLoufrani3,AlainMercat1,2,PaulCalès1,2,PeterRadermacher4,DanielHenrion3,PierreAsfar1,2*, FerhatMeziani2,5,6 Abstract Introduction:Hydrogensulfide(H2S)hasbeenshowntoimprovesurvivalinrodentmodelsoflethalhemorrhage. Conversely,otherauthorshavereportedthatinhibitionofendogenousH2Sproductionimproveshemodynamics andreducesorganinjuryafterhemorrhagicshock.Sinceallofthesedataoriginatefromunresuscitatedmodels and/ortheuseofapre-treatmentdesign,wethereforetestedthehypothesisthattheH2Sdonor,sodium hydrosulfide(NaHS),mayimprovehemodynamicsinresuscitatedhemorrhagicshockandattenuateoxidativeand nitrosativestresses. Methods:Thirty-tworatsweremechanicallyventilatedandinstrumentedtomeasuremeanarterialpressure(MAP) andcarotidbloodflow(CBF).Animalswerebledduring60minutesinordertomaintainMAPat40±2mmHg. Tenminutespriortoretransfusionofshedblood,ratsrandomlyreceivedeitheranintravenousbolusofNaHS(0.2 mg/kg)orvehicle(0.9%NaCl).Attheendoftheexperiment(T=300minutes),blood,aortaandheartwere harvestedforWesternblot(inductibleNitricOxydeSynthase(iNOS),Nuclearfactor-B(NF-B),phosphorylated InhibitorB(P-IB),Inter-CellularAdhesionMolecule(I-CAM),Hemeoxygenase1(HO-1),Hemeoxygenase2(HO-2), aswellasnuclearrespiratoryfactor2(Nrf2)).Nitricoxide(NO)andsuperoxideanion(O2-)werealsomeasuredby electronparamagneticresonance. Results:Attheendoftheexperiment,controlratsexhibitedadecreaseinMAPwhichwasattenuatedbyNaHS (65±32versus101±17mmHg,P0.05).CBFwasbettermaintainedinNaHS-treatedrats(1.9±1.6versus4.4± 1.9ml/minuteP0.05).NaHSsignificantlylimitedshock-inducedmetabolicacidosis.NaHSalsopreventediNOS expressionandNOproductionintheheartandaortawhilesignificantlyreducingNF-kB,P-IBandI-CAMinthe aorta.Comparedtothecontrol