简介:BackgroundAcutecoronarysyndrome(ACS)isaleadingcauseofmortalityandmorbidityworldwide,whichcomprisesunstableangina(UA)andacutemyocardialinfarction(AMI),andtheinvestigationofbiologicalmarkerstoassessthosemostatriskofrecurrentcardiovasculareventsisnecessary.MethodsSixty-sixhealthycontrolpeopleand67casesofUApatientswereenrolledinGuangdonggeneralhospital.Enzymelinkedimmunosorbentassay(ELISA)wasusedtodetectthelevelofplasmaACTG2.Thereceiveroperatingcharacteristiccurve(ROC)wasusedtoanalyzethepredictionvalueofACTG2forUA.AccordingtotheaveragelevelofplasmaACTG2inUApatients,UApatientsweredividedintothelowACTG2group(
简介:BackgroundNowadays,thestudiesmainlyfocusonthefunctionofdecreasingtheinflammatoryfactorandimprovingthefunctionsofendothelium,buttheeffectsofstatinsonventricularremodelingarerarelystudied.MethodsThe2-kindey,1-cliphypertensiverats(2K1C,Goldblatt)werepreparedwithSprague-Dawley(SD)rat.SDratswererandomlydividedintothreegroups:controlrats,hypertensiveratsandhypertensiveratstreatedwithatorvastatin(2mg·kg-1·d-1).After6weeks,systolicbloodpressure(SBP)wasmeasuredusingthetail-cuffmethod.TheplasmaconcentrationofangiotensinⅡandreninactivityweredeterminedbyradioimmunoassay.Theheartweight,theratioofleftventricularweightandbodyweightwascalculated.ResultsTheplasmaconcentrationofangiotensinⅡ(106.4±7.8)ng/Landreninactivity(20.6±2.4)ng/Lweresignificantlyincreaedinhypertensiveratscomparedwithnormalrats[(72.3±5.4)ng/Land(12.5±3.7)ng/L](P<0.01).Theheartweight(1.46±0.09)g,theratio3.54±0.19(×10-3)ofleftventricularweightandbodyweightinhypertensiveratswereobviouslyhigherthanthatinnormalrats[(0.98±0.07)gand(2.28±0.06)×10-3](P<0.01).Aftertreatmentwithatorvastatin,theplasmaconcentrationofangiotensinⅡ(68.3±6.9)ng/Landreninactivity(8.7±2.3)ng/L,heartweight(1.05±0.04)g,theratio2.36±0.07(×10-3)aboveweredecreasedsignificantly,therewerenodifferencebetweenthegroupofhypertensiveratsandthenormal.ConclusionsAtorvastatincandecreasetheratioofleftventricularweightandbodyweightandhastheeffectsoncardiovascularremodelinginhypertensiverats.
简介:ObjectivesTostudyclinicalandcoronaryangiographicfindingsinpatientswithbothcoronaryheartdiseases(CHD)andtype2diabetesmellitus(T2DM).Methods215patientswithCHDconfirmedbycoronaryangiographywereinvolvedinthisstudy.Thepatientsweredividedintotwogroups:74CHDpatientswithT2DM(meanage64.7±8.2years,male/female47/27),and141CHDpatientswithoutT2DM(meanage66.2±9.2years,male/female100/41).Theclinicalfeaturesandthedatafromselectivecoronaryangiographieswerecomparedbetweentype2diabeticandnon-diabeticCHDpatients.ResultsComparedtonon-diabeticCHDpatients,thepatientswithbothCHDandT2DMsufferedmorefromacutemyocardialinfarction,silentischemiaandseverearrhythmias(P<0.01,P<0.05),andhadhigherserumtriglyceridesandapo-lipoproteinB,alongwithincreasedserumuricacid(P<0.01,P<0.05),increasedleftventricularenddiastolicdiameter(P<0.01),anddecreasedleftventricularejectionfraction(P<0.001).Comparedtonon-diabeticCHDpatients,thepatientswithbothCHDandT2DMsufferedmorefromtriplevesseldisease(P<0.01),severecoronaryarterystenosis,completeocclusionsanddiffuselesions(P<0.001).ConclusionsSevereclinicalmanifestation,leftventriculardysfunction,diffuseorcomplicatedlesionsofcoronaryarteriesweremorecommoninpatientswithbothCHDandT2DM,itsuggeststhatthetype2diabeticCHDpatientshavepoorprognosis.
简介:Themyocardialprotectionaffordedbyischemicpreconditioning(IPC)canalleviateischemia-reperfusioninjuryinnormalratheart.However,thismyocardialprotectionisseldomstudiedinthetype2diabeticratwithmyocardialischemiadisease.Inthisstudy,weaimedtoevaluatetheeffectsofATP-sensitivepotassiumchannels(KATPchannels)onIPCintheisolatedtype2diabeticratheartandtheroleofthesulfonylureagliclazide.MethodsStreptozotocin(STZ)-inducedtype2diabeticmaleWistarratswithorwithoutgliclazide(64mg/kgbodyweight,orally)andage-matchednon-diabeticcontrolratswereusedforallstudies.TheisolatedheartswereperfusedwithLangendorff'ssystemundertheconstantflow,pressureandtemperatureconditionswithKreb's-Henseleitsolution(K-H).After5minutesofbalanceperfusion,theseratswererandomlydividedintosixgroups:non-diabeticcontrolratswithoutIPC(CIR);non-diabeticcontrolratswithIPC(CIP);diabeticratswithoutIPC(DIR);diabeticratswithIPC(DIP);gliclazide-treateddiabeticratswithoutIPC(GIR);andgliclazide-treateddiabeticratswithIPC(GIP).GroupsCIR,DIR,andGIRweresubjectedto30-minglobalischemiaand60-minreperfusionforinductionofischemia/reperfusioninjury.GroupsCIP,DIP,andGIPweregiventhreecyclesof5-minischemiaand5-minreperfusionasIPC,andthenischemia/reperfusioninjuryprogramwasimplemented.Extentofischemia/reperfusioninjurywasmeasuredintermsofthereleaseoflactatedehydrogenase(LDH),creatinekinase(CK),andcreatinkinase-MB(CKMB)incoronaryeffluent.Afterperfusion,Kir6.2andSUR2AmRNAexpressionsinthemyocardialtissuewerecharacterizedbyfluorescentquantitativereal-timePCRmethod,andKir6.2andSUR2Aproteinexpressionswereassessedbyimmunohistochemistry.ResultInnon-diabeticcontrolrats,thereleaseofLDH,CK,andCK-MBincoronaryeffluentmarkedlydecreasedwithIPCcomparedwithNo-IPC(P<0.05),butnotindiabeticrats.However,ingliclazide-treateddiabeticrats,IPC-induceddecreaseintherele
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.
简介:目的:探讨2型糖尿病(T2DM)合并高血压与否对脂代谢、微血管病变、血液流变学的影响。方法:192例T2DM患者被分为血压正常组(A组,96例)和合并高血压组(B组,100例),对两组的一般情况、血压、脂代谢、微血管损害及血液流变学情况进行比较分析。结果:B组的血压(148±24)mmHg/(86±15)mmHg、胆固醇(6.0±0.9)mmol/L、血肌酐(70±21.1)μmol/L、血尿酸(343±81)μmol/L和低切粘度(11.02±2.3)均高于A组,有显著性差异(P〈0.05-〈0.01)。结论:T2DM和高血压病均可导致血脂代谢异常,微血管损害和血液流变学的改变,当T2DM合并高血压时,前述异常和损害加重,应及早控制。
简介:目的对中西医结合治疗在2型糖尿病患者中的治疗方式进行讨论。方法选取我院2013年2月-2014年2月间64例2型糖尿病患者,将其分为两组,1组进行常规治疗,2组在进行常规治疗的同时配合中药治疗,对两组患者的治疗效果进行比较。结果1组患者治疗后效果显著的为13例,占比例的40.6%,治疗有效的为14例,占比例的43.8%,治疗无效的患者为5例,占比例的15.6%。2组患者治疗效果显著的为23例,占比例的71.9%,治疗有效的为8例,占比例的25%,治疗无效的仅为1例,占比例的3.1%。结论中西医结合方式治疗2型糖尿病的效果显著,且安全性高,是一种值得推广的治疗方式。
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.