简介：BackgroundRecentstudieshaveshowedthatperivascularadiposetissue(PVAT)maysecretetheadventitial-derivedrelaxingfactor(ADRF)toaffectvascularfunction.However,thefunctionalchangeofADRFinhypertensivestatusisseldomstudied;andthemechanismsofADRFremainunclear.OurstudyexaminedtheADRFsecretedbyperivascularadiposetissueofcontrolratswithnormalbloodpressure(WistarKyotorats,WKY)anddiscussedthemechanismsofADRF;WeobservedthefunctionalchangeinADRFofperivascularadiposetissueinspontaneouslyhypertensiverats(SHRs).MethodThetwoadjacentthoracicaortaringsofSHRandWKYratsweredividedintonakedvesselsubgroupandPVATsubgroup.Thedifferencesofvascularcontractilitybetweenthetwosubgroupsinducedby10-6mmol/Lphenylephrinewerecompared.TheeffectofPVATculturemediumofWKYonthevasculartensionofFat(-)vesselswasobservedbyliquidtransfermeasure.ThemechanismofADRFwasdeterminedbytooldrugs.ResultsInWKYgroup,vascularcontractilityofFat(+)subgroupwaslowerthanthatoftheFat(-)subgroup(P<0.05);whileinSHRgroup,therewasnodifferencebetweenthetwosubgroups(P>0.05).TransferringtheincubationsolutionofWKYFat(+)subgrouptothematchedFat(-)subgroupinducedrapidvasodilation.WhenincubatingbloodvesselsincalciumfreePSSsolution,therewasnosignificantdifferenceofphenylephrine-inducedvasoconstrictionbetweenFat(-)andFat(+)subgroup.Bothglibenclamide,theblockerofATP-sensitivepotassium(KATP)channelandTetraethy-lammoniumchloride(TEA),theinhibitorofcalcium-dependentpotassium(KCa)channel,effectivelyinhibitedvasodilationfunctionofADRF.ConclusionsPerivascularadiposetissueinWKYreleasesADRFwhichcancausevasodilation,whilethisfunctionwasinhibitedinSHR.ADRFactsthroughtheactivationofKCaandKATPchannelsandcalciumionisinvolved.

简介：ObjectivesToquantitativelyanalyzethelongitudinalmyocardialsystolicanddiastolicvelocitiesandtimeintervalsoftheleftventricleinnormalsubjects,andtoexplorethevalueofpulsedDopplertissueimaging(DTI)fortheassessmentofleftventricularsystolicanddiastolicsynchronicity.MethodsTwentyandsixhealthysubjectswerestudiedbypulsedDTI.Theseptalandlateral,anteriorandinferiorwallsoftheleftventricleweredisplayedrespectively,andbasalandmiddlesegmentsofeachwallwereselectedformyocardialmotionspectrumsampling.DTIparameterswere;peaksystolicmyocardialvelocity(s),regionalpre-ejectionperiod(PEP),timetothepeakofswave(Ts),regionalejectiontime(ET);peakearlydiastolicvelocity(e),peaklatediastolicvelocity(a),e/aratio,timetothebeginningofewave(QE),timetothepeakofewave(Te)andregionalisovolumicrelaxationtime(IVRT).ResultsTheeande/aweresignificantlydifferentamongbasalsegments,andsande/aweresignificantlydifferentamongmiddlesegments,withthehighestvalueinlateralsegmentsandthelowestvalueinseptalsegments.Thes,eandawereallsignificandyhigherinbasalsegmentsthanmiddlesegments.Noneofthesystolictimeintervals(PEP,TsandET)anddiastolictimeintervals(QE,TeandIVRT)weresignificantlydifferentamongbasalsegmentsandmiddlesegments,neitherweretheywhenbasalsegmentwascomparedwithmiddlesegment.ConclusionsInnormalsubjects,thelongitudinalmyocardialsystolicanddiastolicvelocitiesoftheleftventriclearenothomogeneous,butthecontractionandrelaxationarehighlysynchronized.PulsedDTIcanbeusedtoquantitativelyanalyzethesystolicanddiastolicsynchronicityoftheheart.

简介：ObjectivesThepurposeofthisstudywastodetermineiftheultrasonicintegratedbackscatterandechointensitycouldbeusedinclinicaldiagnosisofacutemyocardialinfarction.MethodsandResultsWithin2weeksafteracutemyocardialinfarction,35patientsunderwentultrasonictissuecharacterizationfromthepapillaryshort-axisview.Thecyclicvariationofintegratedbackscatterandechointensityofthreedifferentmyocardialregionsperfusedbyleftanteriordescendingcoronaryartery,leftcircumflexcoronaryandrightcoronaryweremeasured.Thevalueofcyclicvariationofintegratedbackscatterandintegratedbackscatterandechointensity≤halfofthehighestvalueofthreedifferentmyocardialregionsonasameviewweredefineasthecriteriafordiagnosingacutemyocardialinfarction,andtheresultswerecomparedwithcoronaryangiography.ThesensitivityofdiagnosingacutemyocardialinfarctionbybothUltrasonictissuecharacterizationwithintegratedbackscatterandechointens

简介：ObjectivesThestudywasperformedtoassesstheleftventricular(LV)regionalandglobaldiastolicfunction,leftventricularwallmotionfeaturesinpatientswithHypertrophiccardiomyopathybyQuantitativeTissueVelocityImaging(QTVI).Methods42patientswithhypertrophiccardiomyopathyand36age-matchednormalsubjectsunderwentQTVIstudy.Off-lineLVregionalmusculartissuevelocityImagingalongLVapicallong-axisviewwereobtained.RegionaldiastolicfunctionwasassessedinusingpeaktissuevelocitiesofLVregionalmusculartissueduringearlydiastole(Ve)andLAcontraction(Va),Ve/Varatio,derivedfromTissueVelocityImaging.Globaldiastolicfunctionwasreflectedbyisovolumicrelaxationtime(IRT)andmitralvalvepeakflowvelocity(E/A)calculatedwithpulsedwavedoppler.Theend-diastolicinterventricularseptalthickness(IVSt)wasmeasuredbyconventional2-dimensionechocardiography.Results①Ve,Va,Ve/Vainthesegmentsofhypertrophicinterventricularseptum(IVS)reducedwlhileE/AratiosignificantlyreducedandIRTmarkedlyprolongedinHCMpatientsthaninnormalsubjects.②Ve,Ve/VaweresignificantreducedinthesegmentsofhypertrophicinterventricularseptumcomparedwithotherLVsegmentsinHCMpatients.③TherewasacorrelationbetweenVe/VaandE/AinHCMpatientswithabnormalE/Aratio(r=0.70).④TherewasanegativecorrelationbetweenVe/VaandIVStinnon-obstructionHCMpatients(Bgroup,r=-0.61)ConclusionsQTVIoffersanewermethodinclinicalpracticewhichhasahighersensibilityandaccuracyinevaluatingtheLVregionalandglobaldiastolicfunctioninHCMpatients.

简介：BackgroundCurrentlyusedheartvalveprosthesesareassociatedwithanticoagulationcomplicationsorlimiteddurability.Theadvancementofstemcellstudyandtissue-engineeredheartvalveresearchmayofferarelativelyidealsolutiontotheseproblems.MethodsBonemarrowwasaspiratedfromsternumoflambgoatstoisolateBMCs.Cellswereidentifiedbyflowcytometryanditscapacityofdifferentiation.CellularviabilitywasassessedwithRhdomine123staining.1×107cellswereseededonapatchofPGAsheet.Aftertwo-dayinvitroculture,theautologouscell/scaffoldsheetswereusedtoreplacetherightposteriorpulmonaryvalveleafletsundercardiopulmonarybypass.Theleafletswereexplantedat2days,2,6,8and10weeksafterimplantation.Thesampleswereexaminedmacroscopically,histologically,immunohistochemically,andbyScanningElectronMicroscope(SEM).Twogoatswereimplantedwithacellularsheetsandestablishedasacontrolgroup.ResultsBMCsexhibitedfibroblastoidmorphologywithgoodviability.FlowcytometryshowednegativeCD14andCD45expression.InvitroculturedBMCsdemonstratedthepotentialtodifferentiateintoadipocytes.Theexplantedleafletsresembledthecharacteristicsofnativeleafletsmacroscopicallyinthecellulargroup.Histologyshowedextracellularmatrixwassynthesizedandcellsweredistributedinthesingle-layeredleaflets.ImmunohistochemistryrevealedpositivestainingforvonWillebrandfactor,α-SMA,vimentin.AconfluentcellsurfacewasformedontheexplantedTEHLs.Nocalciumdepositedontheleaflets.Incontrolgroup,theacellularscaffoldswerecompletelydegraded,withoutleafletremainedat8weeks.ConclusionsItispossibletocreatetissue-engineeredheartvalvesinvivousingautologousbonemarrow-derivedcells.

简介：BackgroundTreatmentofratswiththebeta-adrenergicagonistIsoprenaline(ISO)resultsincardiachypertrophyandmyocardialfibrosis.Inthepresentwork,weaimedtostudytheinvivoeffectsofISOonserumlevelsofmonocytechemoattractantprotein-1andtissueinhibitorofmatrixmetalloproteinasestypeIinWistarrats.MethodsISO(5mg·kg-1)orSalinewereinjectedsubcutaneouslyintoWistarratsonceadayfor3or7consecutivedays.Ventricularremodelingandcardiacfunctionwereevaluatedbyechocardiography.Sectionsofheartwerestainedwithhematoxylin-eosin(HE)forhistopathologyorwithMassonstrichromeforcollagenvisualization.Inaddition,hearttissueimmunohistochemistryforɑ-SMAwasalsoanalyzed.TheserumlevelsoftissueinhibitorofmatrixmetalloproteinasestypeI(TIMP-1)andmonocytechemoattractantprotein-1(MCP-1)weredeterminedbyLuminexmultiplextechnology.ResultsISOinducedcardiacdysfunctioninratsafter3or7daysoftreatment.ISOcausedsignificantincreaseofmyocardialdisorderandfibrosiswithincreasedɑ-SMAexpression.ISOtreatedaatsshowedasignificantincreaseintheserumlevelsofTIMP-1andMCP-1.ConclusionsOurstudysuggeststhatISOinducesprofoundcardiacremodelingaccompaniedwithincreaseofserumTIMP-1andMCP-1.