苯那普利和硝苯地平治疗高血压心脏病——逆转左室肥厚及改善心室舒张功能

用苯那普利（３０例）和硝苯地平（３２例）治疗６２例高血压病人，于治疗前后４周，应用超声心动图检测左室肌重量（ＬＶＭＷ）和左室舒张功能各参数，并与３３例健康成年人作对照。结果显示，两组ＬＶＭＷ及左室舒张功能各参数与对照组比较有极显著性差异（Ｐ＜００１）；苯那普利组治疗前后相比，差异有极显著性（Ｐ＜００１）；硝苯地平组治疗后左室肥厚有回缩，但无显著性差异（Ｐ＞００５），舒张功能参数二尖瓣前叶Ｅ峰至室间隔左室面的距离（ＥＰＳＳ）差异有极显著性（Ｐ＜００１），二尖瓣前叶ＥＦ斜率（ＭＶＶ）、快速充盈分值（ＲＦＦ）、心房充盈分值（ＡＦＦ）有显著性差异（Ｐ＜００５）。提示：苯那普利和硝苯地平对高血压心脏病有良好疗效，且苯那普利优于硝苯地平。     

硝苯地平控释片联合吲哒帕胺治疗老年单纯收缩期高血压52例

目的:评价硝苯地平控释片联合吲哒帕胺治疗老年单纯收缩期高血压的疗效及安全性.方法:选取老年单纯收缩期高血压患者52例,口服硝苯地平控释片30 mg及吲哒帕胺2.5 mg,1次/d,随访13周.结果:治疗后4周患者收缩压明显降低(P＜0.01),波动于正常范围;治疗后13周患者左室肥厚度明显减轻(P＜0.01);治疗后除血钾降低外,肾功能、血脂、血糖无明显变化.结论:联合用药安全、有效,可显著改善左室重塑.     

硝苯地平脉冲片的研制及其体外释药特性

目的 制备硝苯地平脉冲片,考察处方及释放条件对体外释药行为的影响,解析其释放机理。方法 混合粉末直接压片,滚转包衣锅法分别双层包衣(溶胀层和释放衣层)。通过测定释放度研究脉冲片的制剂学特征。结果 双层包衣片以脉冲形式释放,释药时滞随释放衣层厚度增加而延长,释药速率减小;渗透压活性物质和溶胀层可提高快速释放期的释药速率。释放介质pH值和搅拌速度对释药行为无影响。释药机理包括扩散、溶胀和渗透泵机理。结论 调整释放衣膜厚度和组成可获得理想的脉冲释药行为。本给药系统设计可推广应用于水不溶性药物的脉冲给药系统研究。     

硝苯地平控释片与盐酸贝那普利治疗血液透析高血压患者的疗效观察

目的观察硝苯地平控释片（拜新同）及盐酸贝那普利（洛丁新）在血液透析高血压患者中的治疗效果。方法选取2010年1月～2011年12月在本院诊治的68例常规血液透析伴有高血压的患者,随机分为硝苯地平控释片组和盐酸贝那普利组,硝苯地平控释片组36例予以口服硝苯地平控释片治疗高血压（30mg／d,1d2次）,持续4周;盐酸贝那普利组32例予以口服盐酸贝那普利治疗高血压（10mg/d,1d2次）,持续4周,观察并记录两组患者的治疗效果,运用统计学对治疗效果进行统计分析。结果硝苯地平控释片组患者总有效率为94．4％,盐酸贝那普利组患者总有效率为75．0％,硝苯地平控释片组降压效果明显优于盐酸贝那普利组,差异具有统计学意义（P〈0．01）。结论在血液透析伴有高血压患者的治疗方面,硝苯地平控释片的治疗效果明显优于盐酸贝那普利。     

Arsenic-induced alteration in intracellular calcium homeostasis induces head kidney macrophage apoptosis involving the activation of calpain-2 and ERK in Clarias batrachus

We had earlier shown that exposure to arsenic (0.50 μM) caused caspase-3 mediated head kidney macrophage (HKM) apoptosis involving the p38-JNK pathway in Clarias batrachus. Here we examined the roles of calcium (Ca²⁺) and extra-cellular signal-regulated protein kinase (ERK), the other member of MAPK-pathway on arsenic-induced HKM apoptosis. Arsenic-induced HKM apoptosis involved increased expression of ERK and calpain-2. Nifedipine, verapamil and EGTA pre-treatment inhibited the activation of calpain-2, ERK and reduced arsenic-induced HKM apoptosis as evidenced from reduced caspase-3 activity, Annexin V-FITC-propidium iodide and Hoechst 33342 staining. Pre-incubation with ERK inhibitor U 0126 inhibited the activation of calpain-2 and interfered with arsenic-induced HKM apoptosis. Additionally, pre-incubation with calpain-2 inhibitor also interfered with the activation of ERK and inhibited arsenic-induced HKM apoptosis. The NADPH oxidase inhibitor apocynin and diphenyleneiodonium chloride also inhibited ERK activation indicating activation of ERK in arsenic-exposed HKM also depends on signals from NADPH oxidase pathway. Our study demonstrates the critical role of Ca²⁺ homeostasis on arsenic-induced HKM apoptosis. We suggest that arsenic-induced alteration in intracellular Ca²⁺ levels initiates pro-apoptotic ERK and calpain-2; the two pathways influence each other positively and induce caspase-3 mediated HKM apoptosis. Besides, our study also indicates the role of ROS in the activation of ERK pathway in arsenic-induced HKM apoptosis in C. batrachus.     

老年高血压病理生理特点与药物选择的初步探讨

本文对22例老年高血压与23例血压匹配相当的非老年高血压的肾素水平、细胞内离子、血流动力学指标及对药物的降压反应作对比性分析.结果发现,老年组的心输出量、心指数、快速充盈量、血管顺应性降低较非老年组更为明显,外周阻力及细胞内钙含量显著升高,均有统计学差别.细胞内钙含量的升高可能是血管壁僵硬、顺应性降低的分子学基础.在对硝苯吡啶的降压效应方面,老年组血压下降后血流动力学的改善较非老年组为差