5-单硝酸异山梨酯联合美托洛尔治疗冠心病心绞痛疗效观察

目的观察5单硝酸异山梨酯联合美托洛尔治疗心绞痛的疗效。方法采用随机、单盲法将59例心绞痛患者分为两组。治疗组30例,给予5单硝酸异山梨酯联合美托洛尔治疗;对照组29例,给予5单硝酸异山梨酯治疗;观察两组患者用药后各项指标的改善情况并进行比较。结果治疗组总有效率93.3%,对照组为58.6%,组间比较有显著性差异(P<0.01);治疗组心电图改善总有效率66.7%,对照组为40.7%,组间比较有显著性差异(P<0.05)。结论5单硝酸异山梨酯联合美托洛尔治疗心绞痛疗效优于单用5单硝酸异山梨酯。     

The Value of HRV Analysis and Multiple Correlations for Study of Child Virus Myocarditis

Objectives value of HRV analysis and multipl study of child virus myocarditis. To evaluate thee correlations for study of child virus myocarditis.Methods HRV analysis was performed on 41 myocarditis and 40 normal children. The HRV changes in waking and sleeping time were observed as well. Multiple correlation and regression were carried out with the depth of STT depression as dependent variable and all HRV time and frequency domain indexes including those in waking and sleeping time as independent variables. Results HRV abnormality was found in virus myocarditis children .Their HRV indexes were decreased no matter waking time or sleeping time and the differences between waking and sleeping time were muchless than those in the controls. In multiple correlation and regression analysis, the ST depression correlated with VLF, LFN, LF. Conclusions HRV abnormalities existed in children with virus myocarditis which indicates the sympathetic tense were increased permanently. The ST depression correlates with VLF, LFN, LF. HRV analysis is helpful with the study and its diagnosis of autonomic function in children with virus myocarditis.     

罗格列酮抑制内皮素诱发心肌肥大的研究

目的研究罗格列酮（rosiglitazone,RSG）抑制内皮素（endothelin-1,ET-1）诱发心肌肥大的作用及其机制。方法在培养新生大鼠心肌细胞中,采用RSG（PPARγ激动剂）、GW9662（PPARγ抑制剂）和蛋白激酶C（Proteinki-naseC、PKC）通路的激动剂（佛波醇酯,PMA）和蛋白激酶C通路的阻断剂白屈菜季氨碱（chelerythrine、che）观察罗格列酮在ET-1和PMA诱导心肌蛋白质合成中的影响。结果培养2d后,对照组（DMEM）蛋白质含量为（291±13）mg/L,ET-1组和PMA组分别为（339±15）mg/L和（329±14）mg/L,较对照组升高15%和13%（P<0.01）;ET-1+10-7mol/LRSG组、ET-1+10-7mol/LRS组+GW9662组、ET-1+che组、分别为（292±14）mg/L,（310±13）mg/L,（291±17）mg/L;与ET-1组比较分别降低13%、8%、13%（P<0.01,P<0.05,P<0.01）;PMA+10-7mol/LRSG组的蛋白含量较PMA组降低10%（P<0.01）。PMA和ET-1促进心肌细胞蛋白质的合成,RSG和che分别抑制蛋白质合成,PPARγ的阻断剂GW9662减弱RSG的抑制作用。测定心肌细胞的3H-亮氨酸掺入,RSG同样可以抑制ET-1和PMA诱导的心肌细胞肥大,GW9662可以削弱RSG的抑制作用。结论RSG抑制ET-1诱发的心肌肥大与PKC和过氧化物酶增值物激活受体γ（PPARγ）途径可能有一定关系。     

小剂量尿激酶治疗对不稳定型心绞痛患者内皮源性血管活性物质的影响

不稳定型心绞痛（UAP）采用小剂量尿激酶（UK）溶栓治疗临床效果明显。同时，对内皮源性血管活性物质如内皮素．1（ET-1）、组织型纤溶酶原激活物（t-PA）及其抑制剂（PAI-1）也有显著影响，现报告如下。     

过氧化物酶体增殖物激活受体γ与心室重构

研究表明,过氧化物酶体增殖物激活受体γ（PPAR-γ）存在于多种动物的心血管组织内,激活PPAR-γ可改善胰岛素抵抗,影响动脉粥样硬化病变的发生发展,并降低血压。近年来很多研究发现PPAR-γ及其激动剂可以抑制心室重构,但其作用机制有待阐明。     

心脏房室交界区内兴奋传导的组织形态学研究进展

慢径消融是近年来临床治疗某些室上性心律失常的有效方法。作者拟对房室交界区内兴奋传导的组织形态学研究进展做一综述 ,以对慢径消融部位提供形态学参考。     

In-fusion技术构建表达、纯化钠泵α3亚单位膜外区截断性片段重组质粒

目的 构建重组pGEX-6P-1原核表达载体,表达和纯化大鼠钠泵α3亚单位M1～M2和M3～M4膜外区的截断性片段. 方法 利用In-fusion技术将钠泵α3亚单位M1～M2和M3～M4膜外区基因片段插入线性化的pGEX-6P-1载体中,转化,提取质粒,PCR鉴定;用阳性重组质粒pGEX-Trf-α3转化大肠杆菌,IPTG诱导、表达融合蛋白GST-Trf-α3.采用Glutathione Sepharose 4B亲和层析纯化融合蛋白, SDS-PAGE电泳分析表达产物的可溶性及含量.采用放射性配体结合法检测其生物活性.结果 PCR和基因测序分析显示大鼠钠泵α3亚单位M1～M2和M3～M4膜外区被成功插入pGEX-6P-1载体GST基因3′端,蛋白序列分析表明GST-Trf-α3融合蛋白总长度262个氨基酸,理论相对分子质量应约为33.22×103.IPTG诱导后,GST-Trf-α3融合蛋白的表达量为10%,多以可溶性形式存在,可溶性蛋白表达量为80.8%.SDS-PAGE结果 显示其纯度>95%.生物活性实验结果 显示GST-Trf-α3融合蛋白与3H-哇巴因具有一定的结合能力,但结合能力较弱.结论 采用In-fusion技术成功构建了表达GST-Trf-α3融合蛋白的原核表达载体,建立了纯化方法 ,获得高纯度的融合蛋白,为钠泵α3亚单位M1～M2和M3～M4膜外区功能以及其潜在的药理学作用研究获得了实验数据.     

咪唑啉受体在人体内的分布及功能

大量研究表明 ,多种动物的不同组织内均存在咪唑啉受体 ,作用于此类受体 ,可产生多种不同的选择性作用。本文着重阐述了咪唑啉受体在人体内的分布及其功能     

克山病发病与谷胱甘肽过氧化物酶-1基因多态性的关系研究

Objective To assess the association of blood selenium and polymorphism of glutathione peroxidase-1 (GPx-1) genes in patients with Keshan Disease (KD) and provide genetic evidence for KD susceptibility.Methods The levels of whole blood selenium and the activity of GPx-1 were measured with spectrophotometric and enzymatic method among 71 KD patients and 290 controls (including 78 internal controls and 212 external controls).The genotype of GPx-1 at 198 site was analyzed by sequencing and PCRRFLP.The functions of two GPx-1 variants were studied by rat neonatal cardiomyocytes transfection and expression pLamid.Results Blood level of selenium in KD patients was (0.8 ±0.2) μmol/L,the internal controls' was (0.9 ±0.2) μmoL/L,and the external controls' was ( 1.2 ±0.2) μmol/L (F=4.888,P＜0.001 ).GPx-1 activity of KD patients was (73.0 ± 12.6) × 10-10 U/RBC, internal controls' was ( 80.9 ±9.2) × 10-10U/RBC,and external controls' was ( 115.8 ±21.1 ) × 10 -10U/RBC ( F =5.324,P ＜0.001 ).Those of KD patients were significantly lower than controls.The polymorphism (Pro198Leu) of GPx-1 were identified; the frequency of Pro198Leu of KD patients was 21.1% , the frequency of controls was 10.7%(χ2 =5.588 ,P =0.018).The level of blood selenium in variant subgroup( Pro198Leu or Leu198Leu) was(0.9 ± 0.2) μmoL/L, and its in non-variant subgroup was ( 1.1 ± 0.3 ) μmol/L ( t = 3.183, P ＜ 0.01 );The GPx-1 activity in variant subgroup was (86.1 ± 23.0 ) × 10-10U/RBC, and its in non-variant subgroup was ( 101.8 ± 25.9 ) × 10-10 U/RBC ( t = 5.784, P＜ 0.01 ) .Further analysis revealed a synergisticmultiplicative interaction between presence of GPx-1 codon198 alleles and low blood selenium level Overexpression of GPx-1 (198Leu) in rat cardiomyocytes caused 30% lower enzyme activity and less response to increasing concentrations of selenium than with over-expression of GPx-1 (198Pro).Conclusion Low blood selenium in carriers with the 198Leu-susceptible genotype of GPx-1 is associated with low GPx-1 activity,synergistic-multiplicative interaction was found between these two factors.And these two factors may increase the risk of KD.