简介：

简介：Criticalcardiogenicshockremainsaproblemwithstaggeringmortality,withthebesthopeofsurvivaldependingontimelyandaggressiveintervention.Thisoftenrequirestheuseofextracorporealmechanicalsupportinadditiontovasoactivemedicationstomanagepatientsthroughtheirinitialinsult.Thedecisiontousesuchsupportmustbemadeearlyintheclinicalpresentation,andisbestdoneinamultidisciplinaryfashion.Inthisarticle,wereviewtheliteratureandprovideanalgorithmforthetreatmentofcardiogenicshock.

简介：AreviewarticlebyHaoetal.(JAmCollCardiol2017;69(24):2952–66)hashadhugerepercussionsamongthosefamiliarwithtraditionalChinesemedicine(TCM)intheinternationalacademiccommunity.ItevaluatedtheefficacyandsafetyofTCMforcardiovasculardiseaseandthepharmacologicaleffectofactiveTCMingredientsonthecardiovascularsystemandpotentialmechanisms.Wehaveseveralcomments:Firstly,wegiveabriefsummaryaddressingnonpharmacotherapyinTCM,includingacupuncture,moxibustion,Qigong,andTaiChi.Secondly,wehaveaddedtraditionalantiarrhythmicdrug–relatedrandomizedcontrolledtrialstomakethecoveragemorecomprehensive.Lastly,wesupporttheconceptthatresearchinto,developmentof,andapplicationofactiveingredientsispartofmodernTCM.

简介：ObjectivesToexamineinvivointeractionsbetweenangiotensinⅡ(AngⅡ)AT1areceptor(AT1aR),angiotensin-convertingenzymes(ACE)andACE2usingsmallhairpinRNA(shRNA)gene-silencingmethodsinmicebrainstemnucleustractussolitarius(NTS).MethodsC57BLmice(n=8)wereusedasanimalmodel.MethodofmicroinjectioninthenucleusofNTSwasadopted.Aftertendays,micewerekilledandtheirbraintissuewerefixedandsectioned.TheexpressionlevelsofAT1aR,ACEandACE2mRNAatbothsidesofNTSwereexaminedbyinsituhybridization.Basedoncomparedt-test,thechangingformRNAexpressionwasexamined.ResultsAftertheexpressionofAT1aRmRNAwassignificantlyinhibited(61.6%±6.8%)byAT1aR-shRNA,itwasassociatedwithdecreasesinACE2mRNAexpressionfrom(1.05±0.12)μCi/mgto(0.74±0.09)μCi/mg(29.0%±14.5%,P<0.01)onthesamesideofthebrainstem.ACEmRNAexpressionwasconsistentatbothsides(0.50μCi/mg±0.09μCi/mgand0.53μCi/mg±0.08μCi/mg),withinsignificantdifference(P>0.05).ConclusionsThegenesilencingresultshowedthattherewereinteractionsbetweenbrainstemAT1aRandACE2.ACEmRNAexpressionwasnotalteredbyRNAinterferencetreatmentatAT1aR.