西比灵、都可喜治疗椎-基底动脉供血不足的临床研究

目的 观察西比灵、都可喜治疗椎-基底动脉供血不足（VBI）的临床效果.方法 将138例椎-基底动脉供血不足患者随机分为两组：对照组（65例）采用丹参注射液20 ml加入低分子右旋糖酐500ml静脉滴注,每日1次;治疗组（73例）在对照组治疗的基础上加用西比灵5 mg,每晚睡前服,以及都可喜1片,每日2次.两组均治疗14日后观察疗效.结果 治疗组的治愈率、显效率分别是52%和41%,对照组的治愈率、显效率分别是34%和32%,两组比较差异有统计学意义（P〈0.01和P〈0.05）.经颅多普勒超声（TCD）检查发现两组经治疗后椎-基底动脉平均血流速度均明显增加,但治疗组明显优于对照组（P〈0.05）.结论 西比灵、都可喜联合低分子右旋糖酐及丹参注射液治疗VBI疗效显著,是一项值得临床推广的好方法.     

硫酸镁合盐酸氟桂利嗪防治蛛网膜下腔出血后脑血管痉挛的疗效观察

目的:观察硫酸镁合氟桂利嗪防治蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的疗效.方法:将SAH患者88例,随机分为观察组和对照组各44例,.对照组采用脱水、止血等常规疗法;治疗组在常规疗法基础上加用25(硫酸镁60ml加生理盐水250ml,静脉滴注,1次/d;14天后停用,盐酸氟桂利嗪40mg,qn,po.采用经颅多普勒(TCD)检测SAH患者脑动脉的收缩峰速度,观察各组CVS发生的情况.结果:治疗组预防蛛网膜下腔出血后脑血管痉挛疗效于对照组显著改善(P<0.01),观察组总有效率高于对照组(P<0.05),且无明显不良反应。结论:硫酸镁合氟桂利嗪防治SAH后CVS疗效好而且安全。     

沙鼠脑缺血性再灌注及西比灵干预对PAI-1表达变化的影响

目的研究沙鼠脑缺血再灌注后脑内1型纤溶酶原激活物抑制剂(PAI-1)蛋白表达变化,以及西比灵干预的影响。方法制作沙鼠脑缺血再灌注模型,实验前给沙鼠喂食西比灵,分别在缺血再灌注(IR)1、3、7 d,用免疫组织化学方法检测脑内PAI-1蛋白的表达,并与其他各组比较。结果正常对照组与假手术组沙鼠脑组织中有微弱PAI-1的阳性表达。缺血再灌注1、3、7d PAI-1呈阳性或强阳性表达,蛋白的表达随再灌注后时间的延长而递增,7 d达高峰,不同时间点PAI-1的表达差异有统计学意义(P<0.01)。西比灵干预后PAI-1的表达趋势亦同缺血再灌注组,但阳性率高于缺血再灌组,差异有统计学意义(P<0.01)。结论沙鼠脑缺血再灌注可诱导脑组织神经元和胶质细胞表达PAI-1蛋白,西比灵可上调PAI-1蛋白表达而有利于抵御脑缺血再灌注造成的脑损伤。     

盐酸氟桂利嗪对实验性脑出血大鼠体感诱发电位的影响

目的:观察钙拮抗剂盐酸氟桂利嗪对脑出血后神经功能缺失的修复作用。方法:用66只成年健康Wistar大鼠,分为正常对照组(6只)、脑出血组(30只)和治疗组(30只)三个组,对后两组运用胶原酶法建立大鼠脑出血模型,其中出血组仅制模不作处理,治疗组于制模前一天及制模后五天,按1 mg／kg体重腹腔注射盐酸氟桂利嗪,每日一次。此两组均于制模后分别于0．5、6、24、72、120 h五个时点各6只鼠作体感诱发电位(SEP)测定P1-N1蜂峰值、P1波潜伏期值、N1潜伏期及神经功能评定后处死。结果:脑出血后SEP波幅降低和潜伏期延长。治疗组脑出血后6 h波幅开始明显降低及潜伏期明显延长,持续约3天左右后逐渐恢复,SEP的P1-N1峰峰波幅升高及P1、N1波潜伏期缩短,治疗组与出血组结果比较差异有显著意义(P<0．01)。结论:盐酸氟桂利嗪对脑出血动物神经功能缺失有明显的修复作用,即具有脑保护作用。     

氟桂嗪对偏头痛患者脑血流变化的影响

目的　观察氟桂嗪治疗偏头痛患者脑血流的变化及疗效。方法　采用经颅多普勒超声 (TCD)技术 ,检测 6 0例偏头痛患者颅内动脉血流速度 ,并应用氟桂嗪治疗前后作自身对照。结果　偏头痛患者治疗前颅内动脉的平均血流速度 (Vm)明显快于健康对照组 (P <0 .0 1) ;治疗后平均血流速度明显减慢 ,与治疗前比较差异有显著性 (P <0 .0 5 ,P <0 .0 1) ,与健康对照组比较差异无显著性 (P >0 .0 5 )。临床治疗总有效率为 88.33%。结论　氟桂嗪能改善偏头痛患者颅内动脉的机能状态 ,疗效确切     

吡柔比星膀胱内灌注预防膀胱移行细胞癌术后复发

目的：了解吡柔比星(THP)膀胱内灌注预防膀胱移行细胞癌术后复发的疗效及副作用.方法：患者术后1～2周开始行膀胱灌注.治疗组用30 mg THP加入5%葡萄糖溶液40 mL,对照组用30 mg丝裂霉素(MMC)加入0.9%氯化钠溶液40 mL中充分溶解.常规消毒后,置导尿管入膀胱,排空尿液后注入灌注液.治疗组又分为两亚组,一组为保留药物30 min,另一组为保留药物60 min.对照组保留药物60 min.结果：治疗组膀胱移行细胞癌复发率为16.1%,明显低于对照组33.3%(P＜0.01),副作用差异无显著性(P＞0.05).THP两亚组之间疗效及副作用差异均无显著性(P＞0.05).结论：THP膀胱内灌注预防膀胱移行细胞癌术后复发疗效比MMC好,副作用相似,疗效和副作用与保留时间的关系不密切     

Flunarizine inhibits a high-threshold inactivating calcium channel (N-type) in isolated hippocampal neurons

The action of flunarizine on the high-threshold inactivating calcium channel (N-type) in hippocampal neurons of the rat was investigated using the whole-cell voltage clamp technique. Flunarizine reduced the currents at all test potentials, without shifting the peak of the current-voltage relationship along the voltage-axis. The drug did not affect the activation curve, but drastically decreased the slope conductance in the linear region of the current-voltage relationship. Block of the current by flunarizine occurred in a use-dependent way. Flunarizine was without effect when applied intracellulary, and the onset of action, when applied extracellularly, was slow (range of minutes). The Kd for the block by flunarizine obtained after 6 repetitive depolarizations at 0.2 Hz (pulse duration 150 ms) from -90 mV to 0 mV was 0.8 microM. In conclusion, we present electrophysiological evidence that flunarizine blocks the high-threshold inactivating Ca channel of hippocampal neurons of the rat. We discuss the possibility that flunarizine might inhibit neuronal transmitter release by means of this effect.     

Open dose-ranging trial of flunarizine as add-on therapy in epilepsy

A double-blind placebo-controlled crossover trial of flunarizine as add-on treatment in therapy-resistant epilepsy offered significant evidence of efficacy, but the plasma levels of flunarizine were lower than anticipated, probably due to induction of liver enzymes by comedication. An open dose-ranging trial was therefore undertaken to investigate the relationships among dose, efficacy, side effects, and blood level. With basal medication held constant, flunarizine was added at 3-month intervals in increasing doses of 0, 10, 15, 20, and 25 mg daily, or until side effects occurred or marked seizure reduction was obtained. Forty-seven patients completed the trial; all were adults with therapy-resistant epilepsy who had at least 3 seizures per month. All had complex partial seizures, with additional types in 20. Sixteen patients showed a 50% and 24 a 25% reduction of seizure incidence on flunarizine; 6 and 7, respectively, showed a corresponding increase. The greatest seizure reduction, when observed, occurred generally at a daily dose of 15-20 mg. Side effects, chiefly drowsiness and weight gain, increased markedly between 15 and 20 mg daily. Flunarizine administration produced no change in serum levels of comedication, but flunarizine levels were lower in patients taking more than one other drug. Seizure reduction was obtained most consistently in patients with secondary generalized epilepsy or neurologic deficits. The findings confirm the antiepileptic action of flunarizine in humans and justify further trials.     

氟桂嗪对脑梗死患者血清转化生长因子-β1的浓度影响

目的研究氟桂嗪对脑梗死患者血清转化生长因子-β1（Transforming growth factor-betal TGF-β1）的浓度变化影响。方法收集动脉硬化性脑梗死患者60例，随机分成2组，按缺血性脑血管疾病常规治疗，一组治疗中无钙离子拮抗剂治疗，另一组病后第2d始加口服氟桂嗪20mg／d，分2次，连用14d，采用ELISA双抗体夹心酶联免疫吸附法检测患者发病后第1、3、7、14d血清TGF-β1水平动态变化，并与30例健康体检者作对照。结果脑梗死患者血清TGF-β1浓度在第1d均明显低于正常对照组血清TGF-β1水平（P〈0．01），加用氟桂嗪治疗组血清TGF-β1含量在第3、7、14d均明显高于未加氟桂嗪组，有显著差异（P〈0．01）。结论氟桂嗪可能有利于TGF-β1的信号传递，提高脑梗死患者血清TGF-β1水平，有利于抵御脑缺血再灌注造成的脑损伤。     

氟桂利嗪对慢性精神分裂症患者生活质量的影响

目的:探讨氟桂利嗪辅助治疗对慢性精神分裂症患者生活质量的影响。方法:采用双盲对照方法,对96例以阴性症状为主的住院慢性精神分裂症随机分为两组,在原有抗精神病药基础上,分别合用氟桂利嗪和安慰剂,疗程12周,且在治疗前和治疗4、8、12周末应用生活质量综合评定问卷(GQOLI-74),阳性和阴性症状量表(PANSS)与副反应量表(TESS)评定疗效及不良反应。结果:氟桂利嗪组的躯体健康维度、心理健康维度及社会功能维度得分均明显高于对照组,均有显著性差异。结论:氟桂利嗪辅助治疗有利于提高慢性精神分裂症患者的生活质量。