转换酶抑制剂,β—受体阻滞剂和钙离子拮抗剂对高血压临床事 …

３７８例高血压病患者随机分为ＡＣＥＩ治疗组、β－阻滞剂组及ＣａＡ组,分别予开博通１２．５～２５ｍｇ,３次／ｄ,或依那普利５～１０ｍｇ,２次／ｄ;倍他乐克２５～５０ｍｇ２次／ｄ;硝苯吡啶１０ｍｇ,３次／ｄ治疗,目标血压〈１４０／９０ｍｍＨｇ,２周后未达目标血压者加用利尿剂治疗２周,仍高于目标血压者采用以上双联或三联治疗,并归入联合治疗组（７７例）,均经４年临床观察,以心绞痛、心肌梗塞、短暂脑缺血发作     

转换酶抑制剂、β-受体阻滞剂和钙离子拮抗剂对高血压临床事件发生率的影响

378例高血压病患者随机分为ACEI治疗组、β -阻滞剂组及CaA组 ,分别予开博通 12 .5～ 2 5mg ,3次 /d ,或依那普利 5～ 10mg ,2次 /d ;倍他乐克 2 5～ 5 0mg 2次 /d ;硝苯吡啶 10mg ,3次 /d治疗 ,目标血压 <140 /90mmHg ,2周后未达目标血压者加用利尿剂治疗 2周 ,仍高于目标血压者采用以上双联或三联治疗 ,并归入联合治疗组 (77例 )。均经 4年临床观察 ,以心绞痛、心肌梗塞、短暂脑缺血发作及脑卒中为主要临床事件 ,糖尿病、蛋白尿、高脂血症及肾功能不全为次要临床事件。结果各组主要临床事件发生率 (10 .98%～ 11.6 9% )与主要临床事件总发生率 (11.11% )比较无显著差异 (P >0 .0 5 ) ;各组临床事件发生率 (19.5 1%～ 2 1.5 0 % )与临床事件总发生率2 0 .6 3%比较无统计学意义 (P >0 .0 5 )。β -阻滞剂组 (Ⅱ组 )的次要临床事件发生率 11.2 1%明显高于其它 3组 (P<0 .0 5 )。认为ACEI、β -阻滞剂、CaA均可作为抗高血压首选药物 ,以 β -阻滞剂组糖尿病及高脂血症发生率较高。     

辛伐他汀治疗原发性高脂血症疗效观察

辛伐他汀治疗原发性高脂血症30例．8周末胆固醇（TC）下降35．3％,低密度脂蛋白胆固醇（LDL－C）下降46．6％．甘油王酯（TG）下降30．6％．与治疗前比较有显著差异（P＜0．01）,但高密度脂蛋白胆固醇（HDL－C）升高不明显（P＞0．05）。降低TC、LDL—C方面优于非诺贝特组（P＜0．01）,降低TG两者无差异（P＞0.05）,而升高HDL—C方面差于非诺贝特组（P＜0．05）。提示辛伐他汀可作为原发性高胆固醇血症的首选药物。     

31例肥厚型心肌病患者心电图分析

目的探讨肥厚型心肌病患者的心电图特点。方法超声心动图诊断的肥厚型心肌病患者31例,分析其心电图特点。结果ST段改变者25例（80.6%）,冠状T波改变者19例（61.3%）,异常Q波10例（32.3%）,室性早搏8例（25.8%）,其中晕厥者3例。结论ST段改变、冠状T波、异常Q波是肥厚型心肌病患者的主要心电图表现,对室性早搏者应重视。     

消瘀胶囊预防家兔高脂血症形成的实验研究

目的：观察消瘀胶囊对预防家兔高脂血症形成的影响。方法：48只新西兰兔按血清胆固醇（TC）水平平均分成6组，即正常对照组，高脂模型组，消瘀胶囊小剂量组（25mg/kg)，中剂量组（50mg/kg)，大剂量组（100mg/kg)，血脂康组（65mg/kg)。除正常对照组，余各组给予高脂饲料及相应药物，连续服用31天后，测定各组兔空腹血脂水平。结果：消瘀胶囊各组可使兔血清TC，低蛋度脂蛋白胆固醇（LDL－c)显著地低于高脂模型组（P＜0．01）；使血清甘油三酯（TG）下降13．2％－43．6％，尤其大剂量组明显（P＜0．05）；对高密度脂蛋白胆固醇（HDL－c)虽然没有升高作用，但可使TC／HDL－c比值明显下降（P＜0．01）。结论：消瘀胶囊具有预防家兔高脂血症形成的应用。     

Expression of C2A domain of synaptotagmin Ⅰ fusion protein and its imaging in the ischemia-reperfusion rat model

Objective To evaluate myocardial apoptosis with 99Tcm-C2A-GST myocardial imaging using the recombined C2A domain of Synaptotagmin Ⅰ by gene engineering. Methods ( 1 ) The C2A gene was inserted into the prokaryotic glutathione S-transferate (GST) fusion protein expression plasmid pGEX-6P-1. The recombinant plasmid was transformed into E. coli BL21. C2A-GST fusion protein was purified after BL21 was induced with isopropyl-β-D-1-thiogalactopyranoside (IPTG). (2)The activity of fusion protein was identified by cell binding test with fluorescein-5-isothiocyanate (FITC)-C2A-GST. (3) The C2A-GST fusion protein was labeled with 99Tcm using 2-iminothiophene hydrocoride method. Radiochemical purity was determined with thin layer chromatography. (4)99Tcm-C2A-GST (7.4 MBq) was injected to ischemia-reperfusion rat models through tail vein. The image was acquired with SPECT at 1 h after injection, and then hearts were removed, rinsed with saline and dyed with triphenyl tetrazolium coride (TTC). The ischemic myocardium was separated from the viable myocardium and was weighted. Its radioactivity was measured by gamma counting. The difference of uptake of radiotracer between ischemic myocardium and normal myocardium was compared using percentage activity of injected dose per gram of tissue ( % ID/g) with standard deviation. SPSS 12.0 and t-test were used for data analysis. Results ( 1 ) C2A-GST fusion protein wassuccessfully expressed and its relative molecular weight was 3.8 × 104. (2) FITC-C2A-GST binding to apoptotic cells could be observed by fluorescent microscopy. (3) The radiochemical purity of 99Tcm-C2A-GST was (98.90 ±0.43)%. (4)The imaging studies showed that there was focal uptake of radioactivity in the ischemic myocardium. In vitro uptake of 99Tcm-C2A-GST was (2.41 ±0.32) % ID/g by the ischemic myocardium, however 99Tcm-C2A-GST-N-hydroxysuccinimide (C2A-GST-NHS) was (0. 82 ± 0. 24) % ID/g. There was statistically significant difference between those two groups (t = 10. 6, P ＜0.01 ). Conclusion The C2A domain of Synaptotagmin Ⅰ expressed by gene engineering can be used as the tracer for noninvasive detection of ischemic myocardium in the ischemia-reperfusion rat model.     

福辛普利与硝苯吡啶治疗高血压病对患者肾功能的影响

目的　探讨福辛普利、硝苯吡啶单独和联合应用对高血压肾功能的影响。方法　 96例高血压病患者随机分为 2组 ,福辛普利组 (10～ 2 0mgqd 2 3例 ) :硝苯吡啶组 (10mgTid 39例 )。治疗 2周后未达目标血压 (<140 90mmHg)者 ,归入联合治疗组 (单药剂量同前 2组 34例 ,有 6例血压仍不能达标 ,剔除观察 ,实际 2 8例 )。疗程 12个月 ,记录治疗前后肾功能指标变化及治疗后各组平均血压。结果　 (1)治疗后 3组平均血压对比无统计学差异。(2 )治疗后福辛普利和联合治疗组血肌酐和血、尿 β2 -MG均有明显下降 (P<0 .0 1) ;肌酐清除率明显增加 (P<0 .0 1)。 (3)硝苯吡啶组治疗后血肌酐和血、尿β2 -MG虽有所下降 ,肌酐清除率有所增加 ,但未达统计学水平。 结论　福辛普利长期单用或与硝苯吡啶合用 ,在降压同时能有效地降低血肌酐和血、尿 β2 -MG ,增加肌酐清除率 ,保护肾功能     

福辛普利与硝苯吡啶治疗高血压病对患者肾功能的影

目的探讨福辛普利、硝苯吡啶单独和联合应用对高血压肾功能的影响.方法 96例高血压病患者随机分为2组,福辛普利组(10～20mg qd 23例): 硝苯吡啶组(10mg Tid 39例).治疗2周后未达目标血压(<140/90mmHg)者,归入联合治疗组(单药剂量同前2组34例,有6例血压仍不能达标,剔除观察,实际28例).疗程12个月,记录治疗前后肾功能指标变化及治疗后各组平均血压.结果 (1)治疗后3组平均血压对比无统计学差异.(2)治疗后福辛普利和联合治疗组血肌酐和血、尿β2-MG均有明显下降(P<0.01);肌酐清除率明显增加(P<0.01).(3)硝苯吡啶组治疗后血肌酐和血、尿β2-MG虽有所下降,肌酐清除率有所增加,但未达统计学水平.结论福辛普利长期单用或与硝苯吡啶合用,在降压同时能有效地降低血肌酐和血、尿β2-MG,增加肌酐清除率,保护肾功能.