简介：BackgroundAtrialfibrillation(AF)isthemostcommonsustainedcardiacarrhythmiawithouteffectivetreatment.AFisassociatedwithatrialconductiondisturbancescausedbyelectricaland/orstructuralremodel-ing.Buttheroleofconnexin(Cx)43intheregulationofLtypecalciumchannel(LCC)remainsunclear.WehypothesizedthatCx43mightco-localizeandregulatetheLtypecalciumchannelcurrent(ICa,L).MethodsReal-timePCRandwhole-cellpatchclampwereusedtodetecttheexpressionofLCC1csubunitandthecurrentdensityofICa,L,beforeandafterCx43knockingdownrespectively.Theco-localizationofCx43withLCCwasinvestigatedbyco-immunoprecipitationandconfocalmicroscopy.ResultsKnockingdownofCx43significantlyinhibitedthecurrentdensityofICa,LthroughdecreasingthegeneexpressionofLCCα1cinculturedatrium-derivedmyocytes(HL-1cells).Cx43co-localizedwithLCCα1csubunitinatrialmyocytes.ConclusionsCx43regulatestheICa,LinatrialmyoctyesthroughLCC,representingapotentialpathogenicmechanisminatrialarrhythmias.

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.

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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：患者女,66岁。1年前无明显原因出现发作性心前区不适,无心悸、胸闷、头昏、黑蒙等。无高血压、冠心病(冠状动脉造影阴性)及糖尿病等病史。常规心电图(图略),P波顺序出现,P—R间期0.28s,P—P间期0.85s,心率72次/min,一度房室阻滞。发病时心电图(图1)示,P_(1-9)为窦性P波,P—P间

简介：目的探讨L－精氨酸治疗心肌缺血患者的次极量运动试验结果的改善作用。方法用药前后行次极量运动试验观察心肌缺血情况。结果L-精氨酸治疗后运动应激对冠脉血流明显好转。结论L－精氨酸具有缓冲缺血性心脏病在次极量运动负荷时交感神经张力过度增高而导致的心肌缺血的作用。

简介：ObjectivesToinvestigateeffectofAngll,captoprilonsingleguineamyocytesonL-typecalciumcurrentandsodiumcurrent.MethodsMembranepatchclampwholecellrecordingtechniquewasusedtoinvestigateeffectofangll,captoprilonL-Camaximumcurrentdensityandsodiummaximumcurrentdensity.ResutlsAngllincreasedthemaximumcurrentdensitycomparedwithcontrolafterperfused5min,357.7±219.7Vs279.5±240.5PA/PF,increaserateis27.9%,theshapeofcurrent-voltagerelationshipcurvewasunchanged,peakedat+10mv,indicatedthatangllincreasedL-Cacurrentdensityinvoltage-dependent.Afterperfusedwithcaptopril,captopril+angll3,5min,L-Cacurrentwasrecorded,resultssuggestL-Camaximumcurrentdensitydecreasedsignificantlycomparedwithcontrol,incaptoprilgroup,128.4±92.6Vs286.2±89.7,66.7±68.3Vs286.2±89.7,respectively,rateofinhibitionis55.1%,76.6%,respectively.L-Cacurrentfurtherdecreasedincaptoprilpe

简介：目的观察扩张型心肌病（DCM）24h12导联动态心电图改变。方法58例均经心脏超声检查诊断为DCM，再行24h12导联动态心电图监测。结果所有病例动态心电图均有异常改变，以心律失常最为常见。其中室性心律失常56例（96．6％），房性心律失常43例（74．1％），ST—T改变32例（55．2％）、室性心动过速29例（50．0％）。心功能越差，复合性心律失常越多见。传导阻滞25例（43．1％），房室肥大27例（46．6％），Q—T间期延长24例（41．4％），异常Q波8例（13．8％）等。结论DCM有多种心电图表现，其多发、多样性心律失常对DCM早期诊断有重要意义。有复合心律失常的患者有必要进行心脏超声心动图检查。

简介：目的评价L-精氨酸对急性冠脉综合征患者血管内皮功能的影响.方法97例急性冠脉综合征患者被随机分到对照组、维生素C治疗组和L-精氨酸治疗组.所有患者分别于入院时及用药3周后取静脉血,测定血浆一氧化氮(NO)、内皮素-1(ET-1)、C-反应蛋白(CRP)和脂蛋白(a)[Lp(a)]的浓度.结果治疗3周后,L-精氨酸治疗组N0高于对照组(P＜0.05),ET-1、CRP、Lp(a)低于对照组(P＜0.01).结论L-精氨酸能够改善急性冠脉综合征患者血管内皮功能.