简介:ObjectivesToevaluateantihypertensiveefficiencyandsafetyofanewdomesticofL-&N-typeCa^2+antagonist-eilnidipinewithimidaprilasapositivecontrol.MethodsAfter2weeks'placebowashingout,22patientsweretreatedwitheilnidipine5mgdailyand27patientsweretreatedwithimidapril5mgdaily.4weekslater,ifpatient'ssittingdiastolicbloodpressureisover90mmHg,his/herdosagewasdoubledforanother4weeks,theothersmeasuringupremainedtheirdosageunchangedforanother4weeks.Bloodpressure,heartrate,bloodandurineroutineexamination,serumglucose,serumchemicalexaminationincludingtotalcholesterol,triglyceride,HDL,LDL,transaminase,creatineetcandsidereactionswererecordedbeforeandafterthetrial.Datawereanalyzedstatistically.ResultsAfter8weeks'treatment,bloodpressurewassignificantlydecreased(P<0.05)inbothgroups,andthetwomedicineshadsimilarantihypertensiveeffects.Furthermore,thereducingofheartratewasstatisticallysignificantcomparedwithbaseline(P<0.01)inthecilnidipinegroup,butnotintheimidaprilgroup.Thenegativechronotropiceffectofcilnidipinehadlittleeffectoncontinuingthetherapy.Therewerenochangesonbloodandurineroutineexaminationandserumlipid,serumglucose,creatine,transaminaseandetcinbothgroups.Theirsidereactionsweremildandwell-tolerated.ConclusionsCilnidipinehasacon-vincingantihypertensiveeffectsimilartothatofimi-dapril.Especiallycilnidipinemaybeadministeredtopatientswithrelativelymildtachycardia.
简介:BackgroundAldosteroneblockerscouldreducetheincidenceofventriculararrhythmiasinmyocardialinfarction(MI)patientsbyregulatinghyperpolarization-activatedcyclicnucleotide-gatedchannel(HCN)expression.ButthemechanismunderlingHCNexpressionisunclear.MethodsEighteenratssurviving24hourspostMIwererandomlydividedinto3groups:MI,spironolactone,andspironolactone+antagomir-133(miRNA-133suppression).Shamgroupratshadasuturelooselytiedaroundtheleftcoronaryartery,withoutligation.HCN2andHCN4proteinandmRNAlevel,andmiRNA-133levelintheborderzoneofpost-MI1weekmyocardiumweremeasured.ResultsSpironolactonesignificantlyincreasedmiRNA-133levelsanddown-regulatedHCN2andHCN4atbothmRNAandproteinlevelsinpost-MIborderzonemyocardium.Antagomir-133reducedtheeffectsofspironolactoneonHCN2andHCN4proteinlevels.ConclusionsTheresultssuggestthatmiRNA-133isinvolvedinspironolactoneinducedHCNexpression,andpartiallycontributedtopost-MIventriculararrhythmias.
简介:目的观察胰岛素增敏剂文迪雅对老年2型糖尿病病人的疗效和安全性.方法选择血糖控制不佳,胰岛素水平高的老年2型糖尿病病人30例,用文迪雅片4mgqd治疗12周,观察治疗前后血糖及胰岛素的变化.结果治疗后FBG、PBG、GHbAlC、TG下降,与治疗前比较,具有显著性差异(P<0.05),能显著降低FINS、PINS水平(P<0.001),明显改善外周组织对胰岛素的敏感性,治疗后IAI增加,IRI降低,与治疗前比较具有显著性差异(P<0.001),副作用主要为双下肢浮肿和低血糖反应,无肝肾功能损害及胃肠道反应.结论文迪雅降糖效果确切,能降低2型糖尿病病人空腹及餐后2小时血糖,改善外周组织对胰岛素的敏感性,副反应轻微,未见肝肾损害,在老年糖尿病病人中使用具有良好的疗效及安全性.
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.
简介:目的以葡萄糖耐量试验(OGTT)为金标准评价糖化血红蛋白(HbA1c)≥6.5%对于诊断2型糖尿病的可行性。方法对788名无糖尿病史的糖尿病高危患者,行口服75g葡萄糖耐量试验(OGTT),同时检测HbA1c。通过绘制受试者工作特征曲线(ROC曲线),分析HbA1c诊断糖尿病的敏感性和特异性。结果OGTT试验达到诊断糖尿病标准者423例,检出率为54%;而HbA1c≥6.5%者362例(46%)。ROC曲线最佳切点6.35%,此时灵敏度为0.80,特异度0.89。HbA1c≥6.5%时,灵敏度为0.74,特异度0.93,阳性预测值(+PV)93%、阴性预测值(-PV)77%。Kappa检验显示HbA1c≥6.5%与OGTT标准的诊断结果一致性好(Kappa系数为0.68,P〈0.01)。若增加HbA1c≥6.5%这一指标,糖尿病的检出率可增加至57%。结论HbA1c≥6.5%具有很好的敏感性和特异性,可提高2型糖尿病的检出率。
简介:目的探讨血管生成素样蛋白2(ANGPTL2)与急性ST段抬高型心肌梗死(STEMI)患者梗死相关动脉自溶再通的关系.方法选取上游使用替罗非班的STEMI患者88例,根据冠脉造影结果分为自溶再通组43例和未自溶再通组45例(对照组).收集其外周静脉血,通过酶联免疫吸附法检测血浆ANGPTL2浓度,同时提取患者血小板蛋白,利用WesternBlot检测ANGPTL2在血小板上的表达情况.结果STEMI自溶再通组患者外周血血浆中ANGPTL2浓度显著高于未自溶再通组[(37.13±19.49)ng/ml比(26.97±16.91)ng/ml,P=0.011],ANGPTL2在STEMI自溶再通组患者血小板上的表达显著高于未自溶再通组(P<0.05).结论ANGPTL2与STEMI梗死相关动脉自溶再通呈正相关.
简介:BackgroundIncreasedplasmalevelofLp-PLA2isapotentialriskfactorforatherosclerosis.Nevertheless,whetherLp-PLA2haseffectsonbothvascularfunctionandstructurechangesisstillunclear.MethodOnehundredandeighty-sixoutpatientsubjectswithoutovertcardiovasculardiseasewereenrolledandanthropometricdata,plasmalevelofLp-PLA2andotherrelatedlaboratoryparameterswerecollected.Measurementsofpulsewavevelocity(PWV)andcarotidintima-mediathickness(CIMT)wereperformedbyanexperiencedinvestigator.AccordingtoplasmalevelofLp-PLA2,allthesubjectsweredividedintotwogroupsasfollows:<200ng/mL(n=96)and≥200ng/mL(n=90).ResultBodymassindex,smoking,diabeticmellitus,systolicbloodpressure,andLDL-ClevelwerepositivecorrelationwithplasmalevelofLp-PLA2,whileuseofstatinswasnegativelycorrelative.BothPWVandCIMTpositivelycorrelatedwithsmoking,systolicbloodpressure,LDL-ClevelandplasmalevelofLp-PLA2,whilenegativelycorrelatedwithHDL-Clevelandusageofstatins.CIMTinthegroupwithplasmalevelofLp-PLA2<200ng/mL(0.9±0.2mm,n=96)wassignificantlylessthanthatwithplasmalevelofLp-PLA2≥200ng/mL(1.2±0.4mm,n=90,P=0.32),andsimilarfindingwasalsoobservedinPWV(9.1±0.5m/svs12.7±0.4m/s,P=0.38).ConclusionOurpresentstudyshowsthatinsubjectswithoutovertCVD,increasedplasmalevelofLp-PLA2isassociatedwithvascularfunction(PWV)andstructure(CIMT)deterioration.
简介:BackgroundEssentialhypertension(EH)isconsideredtobeoneofthemostimportantriskfactorofischemicstroke.Studiesaboutriskfactorsinthepatientsaremeaningfulinearlyforecastandeffectivepreventionoftheonsetofstroke.Renin-angiotensin-aldosteronesystemplaysanimportantroleintheregulationofbloodpressureandthedevelopmentofstroke,whilerecentstudieshavefoundthattheangiotensin-convertingenzyme2(ACE2)maybeareversalagentforthedevelopmentandprogressionofischemicstroke.MethodsTheACE2genewasmeasuredin139EHpatientswithischemicstrokeusingpolymerasechainreaction(PCR)andrestrictionfragmentlengthpolymorphism(PCR-RFLP)tests.Detailedandcompleteclinicalandbiochemicaldatawerecollected,includingpulsepressure,hsCRP,IMT,HDL-Canduricacidlevels.Studythecorrelationbetweenangiotensin-convertingenzyme2geneandtheriskfactorforonsetofischemicstrokeinEHpatients.ResultsPulsepressure,hsCRP,IMTanduricacidlevelshadapositivecorrelationwithon-setofischemicstrokeinEHpatients.Amongmalepatients,pulsepressure,hsCRP,IMTandHDL-CwerehigherinpatientscarryingAallelethanBallele(P<0.05).Whilethesefactorsweredifferentinfemalepa-tientscarryingdifferentgenotypesinwhichAAallelewerehighest.Patientswithvariousgenotypesshoweddifferenturicacidlevelsbutshowednosignificantdifference.ConclusionAmongEHpatientswithcomplicatedischemicstroke,thosecarryingtheA/AAalleleshowhighlevelofriskfactorsandislikelytohavethesusceptibilityofrecurrenceofstroke.
简介:BackgroundAngiotensinⅡtype1receptor(ATR1)/AngiotensinⅡtype2receptor(ATR2)usuallyinteractwitheachotherintheirexpressionandphysiologicalfunctions,andnitricoxide(NO)isalwaysinvolvedinATR1/ATR2regulationinvivo.Endothelialcellsplayacrucialroleinthemaintenanceofvascularfunctionandinthepreventionofcardiovasculardiseases.ObjectivesToinvestigatetheeffectsofangiotensinⅡ(AngⅡ)andATR1blockervalsartanonATR1,ATR2expressionandtheirrelationwithendothelialnitricoxidesynthase(eNOS)expression,andNOproductioninculturedvascularendothelialcells.MethodsHumanumbilicalveinendothelialcellline(HUVEC)andbovineaorticendothelialcell(BAEC)wereused.BAECwereisolatedfromaortaofnewborncalfbyenzymedigestionandcellsof3-5passageswereused.Cellswereincubatedwithvehicle,AngⅡ,valsartan,orAngⅡplusvalsartanrespectivelyforvariousperiods.ATR1,ATR2,eNOSexpressionandNOproductionweredetected.ResultsIncubationwithAngⅡorvalsartanapparentlydownregulatedATR1mRNAandproteinexpressioninvascularendothelialcells,andthecombinationeffectofthetwodrugsweremoreapparent.AngⅡshowedatransientslightlypromotiveeffectoneNOSandNOgenerationinBAECandanapparentlyinhibitoryeffectwithprolongedincubation,whilevalsartancanapparentlyreversethoseeffects.ConclusionsBothAngⅡandvalsartandownregulatedtheexpressionofATR1invascularendothelialcells.Thesynergisticeffectofthetwodrugswasmoreapparent.ProlongedincubationwithAngⅡcanapparentlyinhibiteNOSexpressionandNOproductioninendothelialcells,whilevalsartancanapparentlyreversethatinhibitoryeffect.