小鼠病毒性心肌炎中Fas/FasL异常表达的研究

目的探讨柯萨奇病毒B3(CVB3)所致小鼠病毒性心肌炎(VM)心肌细胞损伤的变化,观察Fas/FasL介导的细胞凋亡在心肌损伤中的作用.方法采用CVB3制备小鼠病毒性心肌炎动物模型,心肌组织切片HE染色了解心肌损伤情况;电镜检测观察心肌组织中的细胞凋亡;同时采用免疫组化、逆转录-聚合酶链反应(RT-PCR)两种方法检测心肌炎小鼠不同时期心肌组织中Fas与FasL基因转录与蛋白的表达.结果光镜观察见对照组小鼠心肌组织无异常改变,实验组病鼠可见心肌细胞坏死和单核、淋巴细胞浸润,后期可见纤维化;电镜观察对照组心肌中未检出凋亡细胞,而病鼠心肌凋亡细胞检出率较高58.33%(7/12例),且细胞凋亡多存在于炎症病灶周围的心肌细胞及病灶处炎性浸润细胞;感染后第7～14天的病鼠心肌组织中,主要表达于心肌细胞的Fas mRNA及蛋白和主要表达于浸润淋巴细胞的FasL mRNA及蛋白均明显增强;FasL蛋白表达水平与心肌病变积分呈正相关(r=0.9082,P＜0.001).结论小鼠病毒性心肌炎中心肌损伤坏死与心肌细胞凋亡共存,通过Fas/FasL基因路径介导的心肌细胞凋亡与病毒性心肌炎的发病过程有关.     

黄芪对病毒性心肌炎小鼠热休克蛋白70及Bcl-2、Bax基因表达的影响

目的:研究黄芪对病毒性心肌炎(VMC)小鼠热休克蛋白(HSP)70及凋亡相关基因蛋白产物表达的影响。方法:体外培养乳鼠心肌细胞,用Western Blot观察心肌细胞HSP70、Bcl-2及Bax变化;120只Balb/c小鼠随机分为正常对照组、病毒组以及黄芪干预组,采用腹腔接种柯萨奇病毒制做VMC小鼠模型,免疫组化检测各组小鼠Bcl-2和Bax基因表达的情况,并用图像分析系统进行分析。结果:黄芪干预组心肌细胞HSP70及Bcl-2表达明显高于病毒组,2组Bax表达无差异;黄芪干预组心肌组织Bcl-2表达明显高于病毒组,2组Bax表达亦无差异。结论:黄芪可能通过上调心肌细胞Bcl-2、HSP70的表达来抑制病毒所致的心肌细胞凋亡。     

病毒性心肌病小鼠心肌线粒体能量代谢变化研究

目的：观察实验性病毒性心肌病小鼠心肌线粒体能量代谢变化情况，探讨线粒体能量代谢变化在病毒性心肌病发病中的作用。方法：用柯萨奇病毒B3m反复增量感染BALB／C小鼠，建立心肌病动物模型，以荧光分光光度计比色法检测其细胞色素C氧化酶活力。结果：病毒性心肌病组小鼠线粒体氧化磷酸化标志酶细胞色素C氧化酶活力较对照组明显下降（P〈0．05）。结论：心肌线粒体能量代谢障碍是病毒性心肌病的重要病理生理基础。     

银杏叶提取物对大鼠急性心肌缺血再灌注时心肌细胞凋亡及凋亡相关基因表达的影响

目的 探讨银杏叶提取物(EGB)对大鼠心肌缺血再灌注时心肌细胞凋亡及凋亡相关基因表达的影响.方法 采用结扎左冠状动脉前降支(LAD)30 min,再灌注2 h复制大鼠心肌缺血再灌注模型,分别以缺口末端标记法(TUNEL)及免疫组织化学法检测心肌凋亡细胞、心肌细胞Bcl-2、Bax基因的蛋白表达的变化.结果 缺血再灌注(IR)组心肌细胞凋亡数量显著高于假手术组(P<0.01),EGB组心肌细胞凋亡明显受到抑制(P<0.01).IR组和EGB组Bax、Bcl-2、P53基因蛋白表达均明显增加(P<0.01);EGB明显促进Bcl-2基因表达,同时抑制Bax、P53基因表达(P<0.01),Bcl-2和Bax的比值也随之升高.结论 EGB可明显下调Bax和P53基因的蛋白表达,上调Bcl-2基因的蛋白表达,从而显著抑制心肌缺血再灌注损伤(MIRI)后心肌细胞凋亡.     

阿托伐他汀对小鼠病毒性心肌炎心肌细胞凋亡的影响研究

目的:阿托伐他汀钙(atorvastatin)对减少小鼠病毒性心肌炎(VMC)心肌细胞凋亡的影响.方法:4周龄小鼠146只按随机数字法分为4组:正常对照组(正常组,n=18);病毒性心肌炎组(VMC组,n=60);阿托伐他汀钙药物对照组(对照组,n=18);阿托伐他汀钙治疗病毒性心肌炎组(VMC药物治疗组,n=50).VMC组及VMC药物治疗组小鼠腹腔接种柯萨奇病毒,正常组及对照组未注射病毒,VMC组及VMC药物治疗组小鼠给予阿托伐他汀钙,连续用药2周.用药后3、7、10、14、21、30天,苏木素-伊红染色观察心肌组织炎症浸润程度,电镜观察心肌胶原纤维及各种细胞器的变化.缺口末端标记法(TUNEL)检测心肌细胞凋亡情况.反转录酶-聚合酶连锁反应(RT-PCR)及蛋白质印迹方法检测心肌脂肪酸合成酶(Fas)信使核糖核酸(mRNA)和蛋白的表达水平.结果:VMC组比VMC药物治疗组的30 天累计生存率低,差异有统计学意义(P=0.008).VMC药物冶疗组比VMC组在第10、14、21、30天的心肌病理组织学积分均减少,差异有统计学意义(P＜0.05).VMC药物治疗组比VMC组心肌损伤的病灶数量少,心肌线粒体和肌浆网改变也较同期VMC组轻.第14、21天VMC药物治疗组比VMC组凋亡指数降低,差异有统计学意义(P＜0.05).VMC组比正常组Fas mRNA和蛋白的表达均增加,VMC药物治疗组比VMC组Fas mRNA和蛋白的表达均减少,差异有统计学意义(P＜0.05).结论:阿托伐他汀钙改善VMC小鼠生存率,改善组织病理学表现,其机制可能与通过下调Fas转录及表达,从而抑制心肌细胞凋亡有关.表明阿托伐他汀钙对VMC小鼠有明显的保护作用.     

益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响

目的观察益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响,探讨其防治病毒性扩张型心肌病的作用机制。方法采用多次腹腔注射柯萨奇B3m病毒的方式,建立重复感染的早期病毒性扩张型心肌病动物模型。将BALB/c小鼠210只随机分为4组,空白组30只,模型组、中药高剂量组、中药低剂量组各60只。中药高剂量组、中药低剂量组用益气养阴、活血化瘀方治疗4周后,采用原位末端标记法（TUNEL）,观察益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响。结果中药高、低剂量组与模型组相比,可改善小鼠心肌组织病理形态学及超微结构的变化,抑制心肌细胞凋亡。结论益气养阴、活血化瘀方能够减轻病毒性扩张型心肌病小鼠的病理损伤,抑制心肌细胞肥大,抑制心肌细胞凋亡,从而对病毒性扩张型心肌病起到一定的防治作用。     

黄芪总黄酮通过抑制内质网应激对小鼠病毒性心肌炎保护作用的实验研究

目的:探讨黄芪总黄酮对病毒性心肌炎小鼠心肌细胞内质网应激凋亡的作用。方法:将60只雄性Balb/c小鼠均分为病毒性心肌炎组、正常组及黄芪总黄酮组。病毒性心肌炎组与黄芪总黄酮组腹腔内无菌注射含0.1ml 10-9 50TCIDCVB3,正常组不注射CVB3病毒。黄芪总黄酮组小鼠每日腹腔注射20mg·L-1黄芪总黄酮0.2ml,观察小鼠的一般情况,7d时行血流动力学检查后处死取心脏标本,用TUNEL法检测各组小鼠心肌细胞凋亡情况,RT-PCR检测各组小鼠心肌细胞内质网伴侣蛋白GRP78和GRP94的mRNA表达水平。结果:1与正常组相比,病毒性心肌炎组小鼠血流动力学指标明显降低(P0.05);与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠血流动力学指标有显著改善(P0.05)。2TUNEL染色显示,与正常组相比,病毒性心肌炎组小鼠心肌细胞凋亡明显增多(P0.05);与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠心肌细胞凋亡显著减少(P0.05)。3与正常组相比,病毒性心肌炎组小鼠内质网伴侣蛋白GRP78和GRP94的mRNA表达水平均明显升高(均P0.05),且其变化趋势与心肌细胞凋亡数相似;与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠内质网伴侣蛋白GRP78和GRP94的mRNA表达水平明显下降(均P0.05)。结论:黄芪总黄酮对病毒性心肌炎心力衰竭小鼠内质网应激介导的心肌细胞凋亡有保护作用,这可能是黄芪总黄酮改善病毒性心肌炎心力衰竭小鼠血流动力学的作用机制之一。     

EMRE在小鼠心肌缺血损伤中的作用及其相关机制的研究

目的:研究调节线粒体钙单向转运体活性所必须的蛋白(essential MCU regulator,EMRE)在小鼠心肌缺血损伤中发挥的作用及其相关机制。方法:利用心肌点注射EMRE腺病毒(Ad-EMRE)上调心肌组织的EMRE分子表达水平,对照小鼠心肌点注射增强绿色荧光蛋白腺病毒(Ad-eGEP),48 h后,采用结扎小鼠左冠状动脉前降支方法建立心肌梗死(MI)模型。实验设置三组:假手术组(给予Ad-eGFP);心肌梗死对照组(给予Ad-eGFP);心肌梗死处理组(给予Ad-EMRE)。三周后,利用小动物超声系统测定小鼠心脏功能;Western blot及免疫组化检测EMRE分子的表达;麦胚凝集素(WGA)染色检测心肌细胞肥大程度;马松(MASSON)染色检测心肌组织胶原含量;原位末端标记法(TUNEL)检测心肌组织的细胞凋亡;Western blot检测心肌组织半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)和半胱氨酸天冬氨酸蛋白酶-9(Caspase-9)的表达;MitoSOX荧光探针检测线粒体ROS水平。结果:与心肌梗死对照组相比,心肌梗死处理组的心功能明显变差,心肌肥厚明显加重,心肌组织胶原纤维含量更高。另外,心肌梗死处理组的心肌细胞凋亡明显增多,Caspase-3和Caspase-9表达明显升高,线粒体活性氧簇产生也明显增多。结论:EMRE过表达可增加线粒体ROS生成,诱导心肌细胞凋亡,加重心肌缺血损伤。     

病毒性心肌炎心肌超微结构及细胞凋亡的电镜观察

目的研究病毒性心肌炎(VMC)小鼠心肌超微结构改变及细胞凋亡的形态学变化。方法本实验在接种柯萨奇病毒B3(CVB3)建立VMC动物模型的基础上,用光学显微镜及电子显微镜观察心肌细胞的病变及心肌细胞凋亡。结果研究发现实验组小鼠在接种病毒5 d后光镜或电镜下可见心肌病变及炎细胞浸润,7~9 d病变达高峰,35 d时病变基本恢复。VMC小鼠在接种病毒后7~9d,电镜下可见心肌细胞呈凋亡样改变,并可见凋亡小体。结论实验组小鼠在接种CVB3后可引起VMC,VMC中存在异常的心肌细胞凋亡现象。     

慢性心力衰竭大鼠心肌细胞凋亡及Fas基因、FasL(Fas蛋白配体)的变化

目的本实验将探讨腹主动脉缩窄所致慢性心力衰竭大鼠心肌细胞凋亡与Fas及Fas蛋白配体(Fas Ligand, FasL)基因表达的变化,揭示二者与心力衰竭发展过程的关系.方法以腹主动脉缩窄法建立大鼠慢性心力衰竭模型.30只大鼠随机分成假手术组、手术左室代偿性肥厚组(简称肥厚组)及手术心衰组.采用原位末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)观察发生心衰的大鼠和同期仅左室肥厚而未发生心衰的大鼠的心肌细胞凋亡情况,同时以免疫组化ABC显色法分别检测Fas与FasL蛋白水平变化,以逆转录聚合酶链反应法检测Fas基因mRNA的表达改变,从而探讨心肌组织中Fas基因的蛋白与mRNA表达水平与心肌细胞凋亡的关系以及二者在心衰发展过程中的作用.结果假手术组心肌中仅有少许心肌细胞凋亡,实施手术的代偿性肥厚组与心衰组大鼠均有心肌细胞凋亡发生,但心衰组心肌细胞凋亡的数目明显高于对照组.大鼠经腹主动脉缩窄术后4周,左室肥厚而未发生心衰的大鼠其心肌组织Fas蛋白阳性染色指数明显高于假手术组,但Fas配体蛋白阳性染色指数与假手术组间无显著性差异;而发生心衰的大鼠其心肌组织Fas及Fas配体蛋白阳性染色指数明显高于肥厚组,差异有显著性意义(P＜0.05).与假手术组和肥厚组相比较,心衰组心肌组织Fas基因的mRNA表达也上调(P＜0.05).结论实验性心衰大鼠心肌细胞凋亡、Fas基因的蛋白与mRNA表达水平及FasL蛋白表达均增加,心肌细胞出现凋亡可能是心脏由代偿性心肌肥厚向心衰转变过程中的重要机制,心肌组织Fas水平的升高可能与这一改变有关,并可能是其促进因素;心肌细胞凋亡与Fas/FasL系统参与了慢性心力衰竭的发生、发展过程.     

扩张型心肌病心肌纤维化与β-链蛋白表达相关性的初步分析

目的:探讨β-catenin在扩张型心肌病心肌中的表达及其与纤维化的相关性。方法:选取心脏移植术后扩张型心肌病标本15例及法医尸检库正常心肌标本15例做对照;用苏木素-伊红染色观察心肌形态;用Masson染色观察心肌纤维化情况;用免疫组织化学染色显示β-catenin蛋白表达情况;分析β-catenin与扩张型心肌病心肌纤维化之间的相关性。结果:catenin蛋白表达于正常心肌闰盘、血管内皮细胞及活动期的成纤维细胞中,DCM心肌内蛋白可在闰盘处聚集并沿肌丝分布于心肌细胞核两侧的细胞质内。DCM组纤维化区及非纤维化区较对照组β-catenin蛋白表达升高(P均<0.05),DCM组纤维化区与非纤维化区β-catenin蛋白表达差异无统计学意义(P=0.192);DCM组纤维化区纤维化程度较非纤维区及对照组明显(P均<0.001),DCM组非纤维化与对照组区统计学差异(P=0.935);DCM组纤维化区β-catenin蛋白与纤维化程度呈正相关(r=0.681,P=0.005),非纤维化区与对照组β-catenin蛋白与纤维化程度均无明显相关性(P均>0.05)。结论:catenin在扩张型心肌病心肌中表达增高,并与心肌纤维化程度呈正相关关系。     

自身免疫性心肌病抗心肌线粒体腺嘌呤核苷异位酶抗体的动态变化

目的:观察自身免疫性心肌病(AIC)小鼠模型和病毒性心脏病(VHD)患者血清抗心肌线粒体腺嘌 呤核苷异位酶(ANT)抗体的演变规律。方法:建立ANT合成肽AIC小鼠模型,ELISA法定期监测小鼠血清抗 ANT抗体,观察心肌病理变化;对不同病程VHD患者血清进行抗ANT抗体检测。结果:AIC小鼠模型抗ANT 抗体阳性率随着病程延长,呈先上升后下降趋势,病理检查结果提示心肌组织有慢性炎症的改变。在不同病程 VHD患者中,血清抗ANT抗体阳性率也呈现先升高后降低的变化,临床随访发现12.9%病毒性心肌炎转化为 扩张型心肌病。AIC小鼠模型与不同病程VHD患者血清抗ANT抗体演变具有一致性(r=0.53,P>0.05)。 结论:抗ANT抗体水平的变化与心肌病进程相关。     

Histopathological observation of the heart with diffuse and abnormal proliferation of mitochondria in myocardial cells (mitochondrial cardiomyopathy): Report of an adult case

Summary An autopsy case of idiopathic dilated cardiomyopathy with abnormal proliferation of mitochondria in the myocardial cells is reported. The case is that of a 39-year-old male with congestive heart failure. The heart was 700 g and showed marked dilatation of all cardiac chambers with myocardial fibrosis of the left ventricular myocardium and interventricular septum, especially in the basal portion of the left ventricular posterior wall. Myocardial cells were hypertrophied with a marked increase of fine-granular sarcoplasm, containing numerous mitochondria, seen by electron microscopy. The mitochondria were usually round or oval and ranged in size from 0.3 to 1.2 µm in diameter. The cristae of these mitochondria frequently showed a concentric lamellar or reticular configuration. Myofibrils were unusually scarce, but the sarcomere structure and arrangement of myofilaments were well-preserved. Epicardial and intramural coronary vessels were almost normal. From these findings, we consider this to be an adult case of mitochondrial cardiomyopathy.     

Significance of Late Gadolinium Enhancement in Cardiovascular Magnetic Resonance Imaging (CMR)

Cardiovascular magnetic resonance imaging (CMR) permits optimal differentiation between normal and diseased myocardium with the use of gadoliniumbased contrast agents and special magnetic resonance pulse sequences. Imaging is performed 10-20 min after contrast agent application to produce so-called late gadolinium enhancement (LGE) images which depict diseased myocardium with excellent reproducibility. Areas showing LGE correspond to zones of myocyte necrosis or myocardial fibrosis as shown by comparison with histopathology. Typical patterns of hyperenhancement exist in ischemic heart disease but also in dilated cardiomyopathy, hypertrophic cardiomyopathy and other inflammatory or infiltrative myocardial disease and are described in this article. LGE-CMR is helpful to distinguish advanced ischemic heart disease from nonischemic dilated cardiomyopathy. In ischemic heart disease LGE can also predict the functional recovery after revascularization procedures by directly showing the remaining viable myocardium. LGE may also become useful to predict malignant arrhythmias in patients with ischemic heart disease or nonischemic cardiomyopathy. This may lead in future to an increased role of LGE-CMR as a prognostic tool.     

生脉对鼠病毒性心肌病心肌线粒体能量代谢的保护作用

目的：观察生脉注射液对实验性病毒性心肌病小鼠心肌线粒体能量代谢的影响,探讨线粒体能量代谢变化在病毒性心肌病发病中的作用。方法：取Balb／C小鼠,用柯萨奇病毒B3m反复增量感染之,建立心肌病动物模型,生脉干预组小鼠于实验的第60d开始,给予生脉注射液灌胃。存活小鼠：心肌病组（30只）、生脉干预组（36只）。另设正常对照组（13只,给予生理盐水腹腔注射）。104d处死全部小鼠。分别检测3组小鼠心功能及以荧光分光光度计比色法检测其心肌线粒体细胞色素C氧化酶（CCO）活力。结果：病毒性心肌病组小鼠心输出量（CO）[（1.37±0．06）ml／min：（2．13±0．09）ml／min,]、线粒体氧化磷酸化标志CCO活性[（3．06±0．76）k／min·mg：（4．53±1．19）k／min·mg],较正常对照组明显下降（P均〈0．01）;生脉注射组小鼠CO[（1．58±0．07）ml／min：（1.37±0．06）ml／min],CCO活性[（3．98±0．96）k／min·mg：（3．06±0．76）k／min·mg]较心肌病组明显提高（P均〈0．01）。结论：心肌线粒体能量代谢障碍是病毒性心肌病的重要病理生理基础,生脉注射液具有保护线粒体能量代谢作用。     

Functional and structural abnormalities in patients with dilated cardiomyopathy

Passive diastolic properties of the left ventricle were determined in 10 control subjects and 12 patients with dilated cardiomyopathy. Simultaneous left ventricular angiography and high fidelity pressure measurements were performed in all patients. Left ventricular chamber stiffness was calculated from left ventricular pressure-volume and myocardial stiffness from left ventricular stress-strain relations with use of a viscoelastic model. Patients with dilated cardiomyopathy were classified into two groups according to the diastolic constant of myocardial stiffness (beta). Group 1 consisted of seven patients with a normal constant of myocardial stiffness less than or equal to 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a beta greater than 9.6. Structural abnormalities (percent interstitial fibrosis, fibrous content) in patients with dilated cardiomyopathy were assessed by morphometry from right ventricular endomyocardial biopsies. Heart rate was similar in the three groups. Left ventricular end-diastolic pressure was significantly greater in patients with cardiomyopathy (18 mm Hg in group 1 and 22 mm Hg in group 2) than in the control patients (10 mm Hg). Left ventricular ejection fraction was significantly lower in groups 1 (37%) and 2 (36%) than in the control patients (66%). Left ventricular muscle mass index was significantly increased in both groups with cardiomyopathy. The constant of chamber stiffness (beta*) was slightly although not significantly greater in groups 1 and 2 (0.58 and 0.58, respectively) than in the control group (0.35). The constant of myocardial stiffness beta was normal in group 1 (7.0; control group 6.9, p = NS) but was significantly increased in group 2 (23.5). Interstitial fibrosis was 19% in group 1 and 43% (p less than 0.001) in group 2 (normal less than or equal to 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (beta) and interstitial fibrosis (IF) (r = 0.95; p less than 0.001) and beta and fibrous content divided by end-diastolic volume index (r = 0.93; p less than 0.001). It is concluded that myocardial stiffness can be normal in patients with dilated cardiomyopathy despite severely depressed systolic function. Structural alterations of the myocardium with increased amounts of fibrous tissues are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (beta) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.     

Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy.

To investigate how insulin-like growth factor I (IGF-I) modulates cardiovascular function and myocardial apoptosis in heart failure, the therapeutic effects of IGF-I were determined in a canine model of dilated cardiomyopathy. The animals were paced at 220 beats/min, and the left ventricular (LV) chamber became dilated after 2 weeks. A subset of paced dogs was treated with s.c. injections of IGF-I from week 3 to week 4. After 4 weeks of pacing, untreated paced dogs developed significant ventricular dysfunction. IGF-I-treated paced dogs showed better cardiac output, stroke volume, LV end-systolic pressure, and LV end-diastolic pressure. Moreover, pulmonary wedge pressure and systemic vascular resistance were increased in the untreated group and decreased in the IGF-I-treated group. IGF-I treatment was associated with less thinning of the ventricular wall. Compared with the controls, untreated paced dogs showed increased apoptosis of cardiac muscle cells, which was partially suppressed by IGF-I treatment. The myocardial apoptotic index was negatively related to the thickness of the ventricular wall and to cardiac output, suggesting that ventricular remodeling/dysfunction involves the occurrence of myocardial apoptosis. Due to the close resemblance between this experimental model of dilated cardiomyopathy and human heart failure, the results of this study provide evidence that IGF-I may be a potential therapeutic agent for the failing human heart.     

慢性心力衰竭大鼠心肌细胞凋亡及Fas基因、FasL（Fas蛋白配体）的变化

目的　本实验将探讨腹主动脉缩窄所致慢性心力衰竭大鼠心肌细胞凋亡与Fas及Fas蛋白配体 (FasLigand ,FasL)基因表达的变化 ,揭示二者与心力衰竭发展过程的关系。方法　以腹主动脉缩窄法建立大鼠慢性心力衰竭模型。 3 0只大鼠随机分成假手术组、手术左室代偿性肥厚组 (简称肥厚组 )及手术心衰组。采用原位末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法 (TUNEL)观察发生心衰的大鼠和同期仅左室肥厚而未发生心衰的大鼠的心肌细胞凋亡情况 ,同时以免疫组化ABC显色法分别检测Fas与FasL蛋白水平变化 ,以逆转录聚合酶链反应法检测Fas基因mRNA的表达改变 ,从而探讨心肌组织中Fas基因的蛋白与mRNA表达水平与心肌细胞凋亡的关系以及二者在心衰发展过程中的作用。结果　假手术组心肌中仅有少许心肌细胞凋亡 ,实施手术的代偿性肥厚组与心衰组大鼠均有心肌细胞凋亡发生 ,但心衰组心肌细胞凋亡的数目明显高于对照组。大鼠经腹主动脉缩窄术后 4周 ,左室肥厚而未发生心衰的大鼠其心肌组织Fas蛋白阳性染色指数明显高于假手术组 ,但Fas配体蛋白阳性染色指数与假手术组间无显著性差异 ;而发生心衰的大鼠其心肌组织Fas及Fas配体蛋白阳性染色指数明显高于肥厚组 ,差异有显著性意义 (P <0 0 5)。与假手术组和肥厚组相比