不同抗血小板药物治疗不稳定型心绞痛患者血小板聚集功能的观察

目的:比较联合应用阿司匹林(ASA)和噻氯匹啶(TP)与单独应用ASA治疗不稳定型心绞痛(UAP)患者时血小板对不同诱聚剂诱导的聚集性改变及其临床意义。方法:选择UAP患者68例,随机分为ASA组(32例)和联合用药组(36例),服药后14 d应用比浊法测定由二磷酸腺苷(ADP)、花生四烯酸(ACA)和胶原(Coll)(终浓度分别为2.5 mmol/L、1.5 mmol/L、100 mg/L)诱导的血小板聚集功能;正常对照组20例,检测方法同其他两组。结果:联合用药组和ASA组ADP诱导的最大血小板聚集率均显著低于正常对照组(P<0.01与P<0.05),但ASA组仍显著高于联合用药组(P<0.05);联合用药组和ASA组ACA诱导的最大血小板聚集率差异无显著性意义(P>0.05),但均显著低于正常对照组(P<0.01);联合用药组Coll诱导的最大血小板聚集率显著低于ASA组(P<0.01),后者与正常对照组差异无显著性意义(P>0.05)。结论:UAP患者急性期联合应用ASA和TP抑制血小板聚集功能优于单独应用ASA。     

扩张型心肌病与δ-肌聚糖基因关系的研究

目的探讨中国人扩张型心肌病患者中δ肌聚糖基因的突变情况。方法通过聚合酶链反应单链构象多态性分析,结合脱氧核糖核酸测序,对扩张型心肌病患者60例和对照者60例进行δ肌聚糖基因所有9个外显子的分析。结果该基因外显子3发现3种类型单链构象多态性图谱;脱氧核糖核酸测序证实为T84C单核苷酸多态性,所编码氨基酸未发生改变;其等位基因频率在扩张型心肌病组和对照组中差异无显著性（P>0.05）;但在亚组分析中,扩张型心肌病伴传导阻滞亚组T等位基因频率显著高于对照组（P<0.01）。结论中国人群中存在δ肌聚糖基因T84C单核苷酸多态性;该多态性T等位基因是扩张型心肌病伴传导阻滞的易患基因或与心脏传导系统疾病有关。     

106例心脏性猝死的病理和相关因素分析

目的探讨心脏性猝死(SCD)的病理基础及相关因素,为SCD的诊断和防治提供线索。方法回顾性分析我院106例SCD的临床病理资料,分析SCD的病因及年龄,SCD的诱因,各种导致SCD病因的病理改变。结果106例SCD中,冠心病49例,心肌炎15例,心肌病20例,主动脉夹层动脉瘤破裂7例,先天畸形6例,克山病2例,心肌萎缩1例,心脏轻微病变6例。106例SCD中85例具有诱因。冠心病是中老年人SCD的最主要原因。冠心病SCD49例中,冠状动脉粥样硬化血管Ⅳ级狭窄40例,27例呈多支Ⅳ级狭窄;发生急性心肌梗死(简称心梗)10例,其中2例合并陈旧性心梗,单纯陈旧性心梗21例,18例无心梗,仅有心肌缺血。心肌炎和心肌病是中、青年人SCD的主要病因。有6例心脏无明显器质性改变,称之为阴性解剖或青壮年不明原因猝死。结论尽早防治冠心病、监测粥样硬化斑块成分、改善心肌供血是预防中老年SCD的根本措施,减少不良刺激和情感应激对预防SCD有一定意义。在解剖阴性者中进行分子基因筛查,对解释病因和SCD危险分层有重要作用。     

从伦理角度加强医院药理基地管理的实践与体会

药品临床试验是新药开发的重要环节，医院药理基地如何在新药临床研究过程中加强伦理道德规范是关系到每一个受试者权益是否得到保护的大问题，本文从五个方面探讨了加强药理基地过程管理的具体做法和体会，对今后院内药品临床试验规范管理的实施提出了一些措施。     

改善冠心病患者生命质量

第四界国际冠心病会议于2001年10月21日～24日在捷克首都,美丽而古老的山城布拉格举行,来自四十多个国家的近两千名心血管专家就冠心病的分子生物学、发病机制,急性冠脉综合征,冠心病流行病学、预防及预后等多个领域的最新信息进行了广泛的交流和讨论,首次公布了对改善冠心病心绞痛患者生命质量     

容量超负荷大鼠衰竭心室肌细胞肿胀激活内向整流阳离子流 Icir,swell变化的研究

目的探讨肿胀激活内向整流阳离子流Icir,swell在肥大和衰竭(CHF)心室肌细胞的变化.①建立大鼠腹腔动静瘘(ACF)致容量超负荷心力衰竭模型.②采用图文采集及分析系统测量并比较正常和CHF心室肌细胞在等渗(IT)及低渗(0.6T)溶液中体积的变化.③采用全细胞电压钳方式记录正常和CHF细胞在1T及0.6T溶液中体积的变化.     

机械牵张致心肌细胞肥大的信号机制

牵拉培养的心肌细胞能够感知机械牵拉并将其转变为细胞内生长信号从而导致心肌细胞肥大。牵张心肌细胞可能引起血管紧张素Ⅱ（AngⅡ）的快速分泌，AngⅡ与其他生长因子共同调节牵拉所致的心肌细胞肥大反应。本文拟综述牵拉培养致心肌细胞肥大的可能机制。     

Granulocyte-macrophage colony stimulating factor improves cardiac function in rabbits following myocardial infarction

To investigate the therapeutic potency of recombinant human Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) in a rabbit myocardial infarction model. Methods: A myocardial infarction was created by the ligation of the major ventricular branch of the left coronary artery in rabbits. After myocardial infarction, the ani-mals were randomly assigned to GM-CSF treatment group, untreated groups and sham-operated group. The rabbits of the treated group were injected into GM-CSF by subcutaneous administration, 10μg/kg/day, once a day for 5 days.The untreated and sham-operated group received a equal saline in the same manner as treated group. Six weeks later echocardiography and haemodynamic assessment were undertaken to assesse cardiac function. The size of the infarct re-gion of the heart were also studied. Restflts: The untreated group exhibited significant higher left ventricle end-diastolic pressure, higher central venous pressure, and with significant lower mean blood pressure, lower peak first derivative of left ventricle pressure (dP/dt) than the sham group. Also, Rabbits in untreated group display significant systolic dys-function shown by the decreased ejection fraction, diastolic dysfunction shown by increasing in the ratio of E wave to A wave (E/A), and display left ventricle enlargement. However, GS-CSF singnificanfly prevented heart dysfunction, left ventricle enlargement, and reduced infarct size in treatment group. Conclusion: Administration GM-CSF after cardiac infarction can improve heart function. These findings indicate the technique may be a novel and simple therapeutic method for ischemic mvocardium.     

动脉粥样硬化与基质金属蛋白酶

动脉粥样硬化（AS）形成过程也是细胞外基质重构的过程。基质金属蛋白酶（MMPs）是降解细胞外基质最重要的酶类，适度调节MMPs的活性防治AS的发生引起了人们的重视。近年来人们对MMPs的结构功能，活性调节及在AS中的作用有了初步的了解。本文就这方面的研究结果作一综述。     

体外诱导大鼠骨髓间充质干细胞向心肌细胞定向分化的研究

Objective To investigate the role of cardiac myocytes in the differentiation of bone marrow mesenchymal stem cells (MSCs) to cardiac myocytes and the biological properties in the course. Methods The bone marrow of the extremities of the rats was flushed, and bone marrow MSCs were obtained by method of density gradient centrifugation. They were cultured. The second passage of cultured MSCs were labelled with bromodeoxyuridine (BrdU). The cardiac myocytes were obtained from the apex of rat heart with trypsin digestion method, and they were cocultured with labeled MSCs. The developmental changes of bone marrow MSCs were observed under light microscope with immunohistochemical staining for BrdU and a-sarcomeric actin on the 3rd day, anti electron microscopic examination on the 5th day. Results MSCs proliferated fast in primary culture and subculture, positive rate was (90. 34± 2. 31)%, and there was statistical difference when it compared with control group [(4.07±1.35)%, P<0. 01]. The morphology of MSCs changed significantly after coculture. There were new cells nuclei of which were positively stained for BrdU and its cytoplasm positive for actin. Under transmissive electron microscope, sarcomeres like structure and abnormal Z line were observed in cytoplasm. Conclusion Cardiac myocytes can effectively induce bone marrow MSCs to differentiate into cardiac myocytes by coculturing.