简介：目的:观察血小板表面活性蛋白即血小板颗粒膜蛋白(CD63)、溶酶体膜蛋白(CD62P)及血浆C-反应蛋白(C-RP)在不稳定型心绞痛(UAP)发生、发展中的作用及灯盏花的影响.方法:59例UAP患者随机分成灯盏花组(32例)及抵克力得组(27例),并对照观察治疗8周前、后血小板CD63、CD62P及血浆C-RP水平的变化.结果:(1)与健康人及稳定性心绞痛(SAP)对照组比较,UAP患者血小板CD63、CD62P及血浆C-RP水平明显升高(P<0.05,P<0.01);(2)治疗8周后,灯盏花及抵克力得组CD63、CD62P及血浆C-RP测定值分别显著低于治疗前水平(P<0.05,P<0.01),且两组上述各指标水平差异无显著性.结论:血小板活化及炎症反应物在UAP发生及发展过程中起着重要的作用,灯盏花抗血小板活化及减轻炎症反应的突出作用对预防急性冠状动脉综合症的发生和发展有极其重要的临床意义.

简介：目的探讨血小板激活在高血压病与冠心病患者的意义.方法测定正常人和高血压病与冠心病患者血小板表面CD41、CD62p,患者分成A、B、C三组,A组为未经抗血小板治疗的高血压病与冠心病患者37例,B组为正常对照组11例,C组为经抗血小板药治疗的高血压与冠心病患者28例.均取晨空腹静脉血3ml,用FACSCalibur流式细胞仪分析.结果A组CD41、CD41荧光强度和CD62p均高于B组(P＜005),C组的CD41、CD41荧光强度、CD62p均低于A组(P＜005).高血压病组与冠心病组的相关指标比较无显著性差异.结论高血压病与冠心病患者的血小板活化和激活增强,而抗血小板药物(阿司匹林或抵克立得)能抑制血小板激活.

简介：目的心血管造影的记录方法有AOT、录像、激光照片、电影片、CD-R等多种.本文着重介绍电影片记录与CD-R记录方法的比较.

简介：Intherecentpast,bonemarrow(BM)-derivedcellshavebeenusedtoregeneratedamagedcardiovasculartissuespostmyocardialinfarction(MI).Recentclinicaltrialshaveshowncontroversialresultsinrecoveringdamagedcardiactissue.Newprogresshasshownthattheunderlyingmechanismsofcell-basedtherapyreliesmoreheavilyonhumoralandparacrineeffectsratherthanonnewtissuegeneration.However,studieshavealsoreportedthepotentialofnewendothelialcellgenerationfromBMcells.Thus,effortshavebeenmadetoidentifycellshavinghigherhumoralortherapeuticeffectsaswellastheirsurfacemarkers.Specifically,BM-derivedCD31~+cellswereisolatedbyasurfacemarkeranddemonstratedhighangio-vasculogeniceffects.IwillpresentrecentadvancesinthetherapeuticuseofBM-derivedcellsandtheusefulnessofCD31~+cellsasanextgenerationcelltherapy.

简介：ObjectivesToinvestigatethechangeandclinicalsignificanceofclopidogrelonplateletmembraneCD40Lincoronaryarterydiseasepatientsbeforeandafterpercutaneouscoronaryintervention(PCI).Methods30caseswhowerediagnosiscoronaryarterydiseases(CAD)bycoronaryangiography,meanage56±9yearsold.Allthepatientswhohadnoantiplateletaggregationcontraindication,weretreatedwithstandardantianginapectorisdrugs.BeforePCI,allthepatientstookclopidogrel75mgperday.ActivatedplateletmembraneCD40LexpressratewasmeasuredbyflowcytometrybeforeandafterPCI6hours.ResultsActivatedplateletmembraneCD40Lexpressratewere3.73±2.15and2.46±0.90,respectivelyin30patientsbeforeandafterPCI6hours.ActivatedplateletmembraneCD40LexpressratewassignificantlydecreaseafterPCI6hoursthanthatbeforePCI(P<0.01).ConclusionsClopidogrelhassignificanceeffectonplateletmembraneCD40LincoronaryarterydiseasepatientsundergoingPCI.Clopidogrelcansuppressionplateletactivationandpreventthromboembolismeventoccurrence.

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