简介：ObjectivesToinvestigatetheeffectsofadrenergicreceptorantagonist(metoprololorprazosin)onmyocardialα1-ARdensityandthechangesofventriculareffectiverefractoryperioddispersion(VERP-D)inrabbitsaftermyocardialinfarction.Methodstwenty-fouradultmaleNewZealandrabbitsweredividedintofourgroupsatrandom:controlgroup(n=6);MIwithplacebogroup(n=6);MIwithmetoprololgroup(n=6);MIwithprazosingroup(n=6).Therabbitsreceivedcorrespondingdrugsforsevendays,beginningatthefirstdayafterMIandmyocardialα1-ARdensityweremeasuredandmeanwhile,myocardialβ-ARwasalsomeasured.ResultsIntheplacebogroup,thedensityofventricularα1-ARwasincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion36.9±0.2vs27.3±0.9fmolmg-1Pro-1,p＜0.01;α1-ARinischemicregion33.0±0.9vs26.6±0.4fmolmg-1pro-1P＜0.01).Inthemetoprololgroup,itwasalsoincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion44.7±1.5vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion33.6±0.5vs26.6±0.4fmolmg-1pro-1,P＜0.01).Meanwhilethedensityofventricularα1-ARinnormalregioninthemetoprololgroupwasincreasedincomparisonwithplacebogroup(44.7±1.5vs36.9±0.2fmolmg-1pro-1,P＜0.01).Whileitdecreasedintheprazosingroupincomparisonwithcontrolgroup(α1-ARinnormalregion22.5±0.6vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion20.9±0.4vs26.6±0.4fmolmg-1pro-1,P＜0.01).VERP-DwasincreasedafterMI(P＜0.01).Aftertreatmentwithmetoprololorprazosin,VERP-Dwasdecreased(P＜0.01).ConclusionsAfteracuteMI,α1-ARofventricularmyocardiumwasupregulated,whichmaybeaccompaniedbyitsactivitation.Thedensityofmyocardialα1-ARbecameupregulatedmoredramaticallytreatedwithmetoprololanddownregulatedwithprazosin.Whentreatedwithmetoprololorprazosin,VERP-Ddecreased.

简介：BackgroundThisstudytestedthehypothesisthatmoderatealcoholintakeexertsitscardioprotectiveeffectmainlythroughanincreaseintheserumlevelofhigh-densitylipoproteincholesterol.MethodsandResultsIntheCohortofNorway(CONOR)study,149729adultparticipants,recruitedfrom1994to2003,werefollowedbylinkagetotheCauseofDeathRegistryuntil2006.Atrecruitment,questionnairedataonalcoholintakewerecollected,andtheconcentrationofhigh-densitylipoproteincholesterolinserumwasmeasured.UsingCoxregression,wefoundthattheadjustedhazardratioformenfordyingfromcoronaryheartdiseasewas0.52(95%confidenceinterval,0.39-0.69)whenconsumingalcoholmorethanonceaweekcomparedwithneverorrarely.Theratiochangedonlyslightly,to0.55(0.41-0.73),aftertheregressionmodelincludedtheserumlevelofhigh-densitycholesterol.Forwomen,thecorrespondinghazardratioswere0.62(0.32-1.23)and0.68(0.34-1.34),respectively.ConclusionsAlcoholintakeisrelatedtoareducedriskofdeathfromcoronaryheartdiseaseinthefollow-upofalarge,population-basedNorwegiancohortstudywithextensivecontrolforconfoundingfactors.Ourfindingssuggestthattheserumlevelofhigh-densitycholesterolisnotanimportantintermediatevariableinthepossiblecausalpathwaybetweenmoderatealcoholintakeandcoronaryheartdisease.

简介：BackgroundIt'sestablishedthatLectin-likeoxidizedlow-densitylipoproteinreceptor-1(LOX-1)isinvolvedinintimalhyperplasiaafterballooninjury.Therecentevidencealsosuggeststhatvalsartanhasanantiatheroscleticeffect.Inthisstudy,theexpressionofLOX-1andtheeffectofvalsartanonitsexpressionwasinvestigatedinrataortaafterballooninjury.MethodsRatmodelofaorticendothelialdenudationwasinducedby2Fballooncatheter.Ratswererandomlydividedintothreegroups:control,operationandvalsartantreatment.Theaortictissuesweretakenfromratsineachgroupondays14and28aftersurgery.ThethicknessofvascularwallwasmeasuredwithHEstain,LOX-1mRNAandproteinweredeterminedbyreversetranscription-polymersechainreaction(RT-PCR)andimmunohistochemistry,respectively.ResultsComparedwiththecontrolgroup,significantintimalthickeningwasobservedatday14and28afterinjury.Comparedwiththeoperationgroup,intimalthicknessofeachtimepointwassignificantlydecreasedinvalsartantreatmentgroup.Atday14and28afterballooninjury,theexpressionlevelsofLOX-1mRNAandproteinweresignificantlyincreased,andweregreatlydecreasedaftervalsartantreatment.ConclusionsTheexpressionofLOX-1isincreasedafterendothelialinjury.Valsartaninhibitsaorticintimalthickeninginducedbyendothelialdenudation,whichisassociatedwiththedownregulationofLOX-1expression.