溶栓药对心肌梗塞再通的研究

本文叙述纤维蛋白非特异性及特异性溶栓药的作用机理及特点，梗塞后开始治疗的时间与死亡率的关系；并介绍了阿斯匹林与溶栓药合用的增效作用。     

3-胺基苯丙酮、1-苯基-3-胺基丙醇类化合物的合成及其生物活性

本文合成了10个3-胺基苯丙酮(Ⅴ_(a-e))及1-苯基-3-胺基丙醇(Ⅵ_(b-e'))类新化合物。初步药理实验表明:Ⅴ_(a-e)均具有不同程度的正性肌力作用,其中Ⅴ_a的PEC_(50)为4.3±0.7(%),Ⅵ_(b-e')均具有较弱的负性肌力作用,其中Ⅵ_d还具有较强的利尿作用。     

抗心律失常药的近况和发展方向

开发抗心律失常药以延长心肌支作电位时程的Ⅲ类药为主。一项较大规模的临床试验表明。，ｄ－索他洛尔有致尖端扭转型室性心动过速（Ｔｏｒｓａｄｅ ｄｅ ｐｏｉｎｔｄｓ，简称Ｔｄｐ）的副作用。高度选择性阻断快速激活的钾通道组分（Ｉｋｒ）的Ⅲ类抗心律失常药，不仅有此不良反应，尚有负性频率效应，心率快时药效减弱；还有药效学的局限性，如对缺血性、儿茶酚胺及毒毛药苷Ｇ引起的心律失常均无效。本文讨论了当前心律失常新药     

葛根素对抗H2O2引起血管平滑肌细胞凋亡及坏死

目的：研究葛根素对过氧化氢引起无血清培养的小牛主动脉血管平滑肌细胞凋亡和坏死的影响。方法：通过体外细胞培养，以噻唑兰（MTT）法测定细胞存活率，用流式细胞术检测细胞DNA含量及凋亡细胞百分率；DNA琼脂糖凝胶电泳法观察细胞凋亡过程中DNA断裂程度。结果：H2O2诱导无血清培养的平滑肌细胞凋亡，葛根素可显著降低平滑肌细胞中凋亡细胞百分率，并减少凋亡细胞DNA断裂，同时也减少其引起的平滑肌细胞坏死。结论：葛根素可对抗H2O2引起的无血清培养的血管平滑肌细胞凋凋亡及坏死。     

马尾树中两个非对映异构的三萜与木脂素聚合物和与它们生源相关的三萜咖啡酯

应用RP-HPLC测定兔静注吡洛地尔(15mg/kg)血药浓度,样品用正庚烷提取。流动相以10％三乙胺-甲醇液(甲醇-水=9:1)=5:95。紫外检测波长为254nm,回收率81.4％,日内和日间的RSD值为     

温度对荧光检测5-羟色胺及5-羟吲哚乙酸的影响

荧光分光法检测生物标本内5-羟色胺(5-HT)及5-羟吲哚乙酸(5-HIAA)具有效率高、灵敏度比较满意的优点。用邻苯二甲醛(OPT)法,检测荧光温度一般采用100℃,亦有采用低于100℃的。经研究,荧光检测5-HT与5-HIAA的灵敏度,在60—80℃为好,尤以80℃为最佳反应温度。在100℃时,5-HIAA的检测灵敏度已下降到0℃水平。实验如下: 各试管按下列各项依次加试液(单位为ml),然后在不同温度下反应。     

Effect of 86017 on potassium channels in isolated guinea pig ventricular myocytes

AIM: To comfirm a blockade on potasaiam channel by 86017, a new anti-arrhythmic agent under development. METHODS: Both whole-cell inward rectifier potassium current(I_(k1)) and delayed outward potassium current (I_k)     

Impairment of contraction and release of nitric oxide in rat arota by levothyroxine

AIM: To study the influence of levothyroxine on rat aorta contraction and nitric oxide (NO) release. METHODS: levothyroxine was administered 0.75 mg·g~(-1)×8d sc,and responses of isolated rat aorta rings were recorded and compared in the absence and presence of L-Argnine (LArg) and N~ω-Nitro-L-Argnine(L-NOARG) on norepinephrine (NE)-induced contraction. RESULTS: AUC     

Current and Future Therapeutic Agents in the Man—agement of Heart Failure

Congestive heart failure is a disease in which initially compensatory changes in car-diac, vascular, and renal functions become detrimental over time. The changes are mediated bg a largenumber of neurohormones and cytokines. Counter-regulatory hormones also play a role, but are general-ly insufficient to offset the adverse effects of the neurohormones or progression of the disease. Symp-toms of heart failure occurs in the presence of systolic dysfunction, usually documented by a decrease inejection fraction, or can present with impaired diastolic function occasionally labeled as heart failurewith preserved systolic function of the left ventricle. Heart failure and its treatment represent a medicalproblem of significant importance because of the high mortality associated with it despite the current ther-apy, which has substantial evidence of reduction in mortality and morbidity. Prevention or slowing of theprogressive deterioration in function of the heart and other organs involved through utilizing new