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.
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: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:目的检测2型糖尿病(T2DM)、糖耐量异常(IGT)、空腹血糖受损(IFG)患者肱动脉内皮功能的变化与血小板活化程度的关系。方法分别选取老年T2DM(T2DM组)、IGT(IGT组)、IFG(IFG组)患者和健康体检者(对照组)各20例,空腹静脉血测定空腹血糖(FPG)、TG、TC、HDL-C、LDL—C、糖化血红蛋白(HbA1c)、血小板膜糖蛋白CD61和CD62P。采用高分辨率血管外彩色超声测定肱动脉血流介导的血管扩张功能(FMD)和含服硝酸甘油后肱动脉内径变化(NTG)。结朵T2DM组、IGT组、IFG组FMD较对照组明显下降,而T2DM组NTG较IGT组、1FG组、对照组明显下降(P〈0.05)。多因素线性相关分析,FMD与FPG、TG、TC、LDL-C呈负相关。T2DM组、IGT组、IFG组CD61和CD62P较对照组明显升高(P〈0.05)。CD61与FPG、TC、HbA1c、LDL-C呈正相关,与HDL-C呈负相关;CD62P与FPG、TG、TC、HbA1c、LDL-C呈正相关,与HDL-C呈负相关。FMD与CD61、CD62P呈负相关。结论内皮功能损害和血小板活化在T2DM前期就已经存在,两者互相促进。
简介:目的观察白藜芦醇对高糖诱导的乳鼠心肌细胞凋亡及损伤的影响,探讨硫氧还蛋白(Trx)系统在此过程中的作用。方法使用培养的乳鼠心肌细胞,随机分为三组:正常对照组(葡萄糖5.5mmol/L)、高糖组(葡萄糖25mmol/L)和高糖+白藜芦醇组(葡萄糖25.0mmol/L,白藜芦醇30.0umol/L)。白藜芦醇组给予白藜芦醇30umol/L预处理45min,对照组和高糖组均给予等量相应溶剂处理。各组细胞于正常糖浓度DMEM或高糖DMEM中继续培养48h后,收集上清液和细胞裂解液进行后续研究。结果与正常对照组相比,高糖组细胞乳酸脱氢酶漏出和细胞凋亡明显增加。进一步分析发现,高糖组细胞p38激酶活性、细胞内活性氧生成量,丙二醛(MDA)含量和3一硝基酪氨酸生成量明显升高,Trx活性降低,但其表达未见明显改变,其内源性抑制蛋白硫氧还蛋白相关蛋白(TXNIP)表达增加。白藜芦醇预处理显著减轻了高糖诱导的细胞凋亡及损伤,m活性得到改善,高糖引起的TXNIP表达明显下调,细胞p38激酶活性、细胞内活性氧生成、MDA含量、3一硝基酪氨酸生成量明显降低。结论白藜芦醇对高糖诱导的乳鼠心肌细胞凋亡和损伤具有明显保护作用,其机制与白藜芦醇减少Trx的硝基化,抑制高糖诱导的TXNIP表达上调,从而保护Trx的功能,减少自由基损伤和凋亡的发生有关。
简介:目的观察替米沙坦对老年高血压病患者降压疗效和对糖、脂代谢的影响。方法选择95例60岁以上的老年高血压病患者,停用其他降压药物2周以上,口服替米沙坦治疗8周,观察治疗第4周和第8周与治疗前相比的血压、血糖、胰岛素、糖化血红蛋白及血脂水平。结果与治疗前比较,替米沙坦治疗4周后血压及24h动态血压均有显著下降(P〈0.05)。治疗后血糖、血清胰岛素、糖化血红蛋白明显降低(P〈0.05)。血清胆固醇、甘油三酯、低密度脂蛋白胆同醇水平显著下降(P〈0.05),高密度脂蛋白(HDL)显著上升(P〈0.05)。结论替米沙坦除了有较好的降压效果外,还可以改善糖代谢和脂代谢,对于老年高血压病患者尤其是代谢紊乱者有较好的疗效。
简介:目的本研究旨在观察钙敏感受体(calcium-sensingreceptor,CaSR)在高糖诱导H9C2心肌细胞中的表达以及其对氧化应激的作用.方法将H9C2细胞在不同条件下干预24h,包括正常糖浓度组(NG组)、高糖组(HG组)、高糖+CaSR激动剂组(HG+GdCl3组)、高糖+CaSR抑制剂组(HG+NPS2390组).用CCK8试剂盒检测细胞存活率;DCFH-DA荧光探针检测细胞内活性氧簇(ROS)含量;用比色法检测细胞超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性以及丙二醛(MDA)含量.用Westernblot检测细胞CaSR蛋白表达水平.结果细胞存活率呈糖浓度依赖性降低[(89.00±1.54)%比(98.83±0.47)%,P<0.01],CaSR蛋白表达量呈糖浓度依赖性增加2.14±0.09比1.06±0.05,P<0.01).高糖诱导可使细胞发生氧化应激,SOD(14.14±0.57比22.86±0.58,P<0.01)与GSH-Px(2.62±0.59比3.04±0.89,P<0.01)活性降低,ROS(0.040±0.002比0.020±0.001,P<0.01)与MDA(0.83±0.05比0.54±0.02,P<0.01)生成增多.与HG组相比,HG+GdCl3组细胞氧化损伤加重(P<0.05).而HG+NPS2390组细胞氧化损伤减轻(P<0.05).结论高糖能上调CaSR蛋白表达进而促进氧化应激的发生.