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简介：ObjectivesNitroglycerine(NTG)enhancescoronarybloodflowtocompromisedmyocardiumisimportantinrelievingischemia.However,themechanismforthisincreaseinmyocardialbloodflow(MBF)isnotwelldefined.Insmallvesselsandcapillaries,relativebloodviscosityplaysaveryimportantroleindeterminingmyocardialvascularresistance(MVR).MVRreduceisduepartlytotheincreaseinnegativechargeoferythrocytesurface.WethereforehypothesizedthattheenhancementofnutrientbloodflowtozonesofmyocardialischemiaduringNTGispartlysecondarytoreducedMVRandbloodflowviscosity.Thelatterisaffectedbythenegativechargeoferythrocytesurface.Methods6dogswithLADflow-limitingstenosis(group1)and6dogswithLADflow-limitingstenosisandLCxoccmusion(group2)werestudied.AtbaselineandduringintracoronaryinfusionsofNTG(0.3-0.6μg·kg-1·min-1),hemodynamics,MBF(mL·min-1·g-1),wholebloodviscosity(WBη,mPa.S),elongationindex(EI),eletrophoreticmobilityoferythocytes(EME,[μ.s-1)/(V.cm-1)])andpercentwallthickening(%WT)weredetermined.MVRwascalculatedusingdrivingpressure/MBF.ResultsAscomparedtobaseline,nochangesinhemodynamicswereseenduringNTG.MBFincreasedandMVRdecreasedsignificantlyinnormalbed,thecentral25%andtheentireofstenosedbed(P<0.05),withadecreaseinWBηinbothgroup1andgroup2dogs(18.6±9.7%and19.2±14.5%,respectively).However,the%decreaseinWBηwasproportionedtothe%increaseinMBForthe%decreaseinMVRonlyinthecentral25%ofstenosedbed(r=0.87,P<0.001),butnotintheentirestenosedbedandnormalbed.EIdidnotshowstatisticallysignificantdifferencesbetweenduringNTGandatbaseline,butEMEdidincrease.Andthe%decreaseinWBηduringNTGwasrelatedtothe%increaseinEME(r=0.83,P=0.01).ConclusionsNTGreducedmyocardialvascularresistanceandbloodviscosityduetothechangeofnegativechargeoferythrocytesurfacemay,inpart,bethe

简介：ObjectivesTheeffectsofcarvediloloncalciumcurrent(ICa)wereinvestigatedinisolatedadultratventricularmyocytes.MethodsICawasrecordedbyusingwhole-cellpatch-clamprecordingtechnique.ResultsCarvedilolreversiblyinhibitedICainaconcentration-dependentmanner,carvedilolat0.1,0.3,1and10μmol/LintheextracellularsolutiondecreasedpeakICaby1.52%,18.04%,37.34%and72.18%,respectively.Thesteady-stateinactivationcurveofICawasshiftedtomorenegativepotentials,whiletheactivationcurvewasnotaltered.Therecoveryfrominactivationwasshiftedtorightdirection,itcouldnotberecoveredcompletely.Inaddition,Pretreatmentofventricularmyocyteswithprazosinandpropranololcouldn'tblockthecarvedilol-inducedreductionofICa.ConclusionsCarvedilolinhibitsICainadultratventricularmyocytesbymechanismsinvolvingpreferentialinteractionwiththeinactivatedstateofcalciumchannel.