度洛西汀治疗持续性躯体形式疼痛障碍临床研究

目的观察度洛西汀治疗持续性躯体形式疼痛障碍临床疗效和药物不良反应。方法78例持续性躯体形式疼痛障碍患者按给药时间的不同，分为治疗组30例和对照组48例。治疗组给予度洛西汀；对照组给以氟西汀加小剂量阿米替林治疗。分别于治疗的2、4、6周评定对比2组的疼痛量表（MOSPM）、汉密尔顿抑郁量表（HAMD）和不良反应量表（TESS），观察疗效及其药物不良反应。结果2组患者在治疗的2、4、6周MOSPM疼痛缓解率和HAMD评分差异无统计学意义（P〉0．05）。治疗组于治疗的2、4周TESS评分明显低于对照组，差异有统计学意义（P〈0．01）。结论度洛西汀治疗持续性躯体形式疼痛障碍疗效相似于氟西汀加小剂量阿米替林，但药物不良反应明显降低。     

米氮平与氟西汀治疗抑郁症疗效对照分析

目的:比较米氮平与氟西汀治疗抑郁症疗效和安全性。方法:将60例抑郁症患者随机分为米氮平组与氟西汀组,两组疗程均为6周,采用两者HAMD量表及副反应表(TESS)进行疗效和不良反应评定。结果:米氮平组与氟西汀组的总有效率分别为86.7%和90.0%,治愈率各为63.3%和56.7%,两组间疗效比较差异无显著性。结论:米氮平与氟西汀治疗抑郁症疗效相当且安全性较好。     

电针对抑郁症患者氟西汀副作用的影响

通过设立观察组与对照组,观察在治疗抑郁症过程中,电针对氟西汀副作用的影响,结果显示,电针对氟西汀的副作用具有一定的改善作用,且随着用药时间的延长,其作用更为明显。     

Fluoxetine, but not other selective serotonin uptake inhibitors, increases norepinephrine and dopamine extracellular levels in prefrontal cortex

RATIONALE: The selective serotonin uptake inhibitor (SSRI) fluoxetine has been shown to not only increase the extracellular concentrations of serotonin, but also dopamine and norepinephrine extracellular concentrations in rat prefrontal cortex. The effect of other SSRIs on monoamine concentrations in prefrontal cortex has not been thoroughly studied. OBJECTIVE: The aim of this study was to compare the ability of five systemically administered selective serotonin uptake inhibitors to increase acutely the extracellular concentrations of serotonin, norepinephrine and dopamine in rat prefrontal cortex. METHODS: The extracellular concentrations of monoamines were determined in the prefrontal cortex of conscious rats using the microdialysis technique. RESULTS: Fluoxetine, citalopram, fluvoxamine, paroxetine and sertraline similarly increased the extracellular concentrations of serotonin from 2- to 4-fold above baseline. However, only fluoxetine produced robust and sustained increases in extracellular concentrations of norepinephrine and dopamine after acute systemic administration. Fluoxetine at the same dose blocked ex vivo binding to the serotonin transporter, but not the norepinephrine transporter, suggesting that the increase of catecholamines was not due to non-selective blockade of norepinephrine uptake. Prefrontal cortex extracellular concentrations of fluoxetine at the dose that increased extracellular monoamines were 242 nM, a concentration sufficient to block 5-HT(2C) receptors which is a potential mechanism for the fluoxetine-induced increase in catecholamines. CONCLUSION: Amongst the SSRIs examined, only fluoxetine acutely increases extracellular concentrations of norepinephrine and dopamine as well as serotonin in prefrontal cortex, suggesting that fluoxetine is an atypical SSRI.     

Acute treatment with the cyclic antidepressant desipramine,but not fluoxetine,increases membrane-associated G protein-coupled receptor kinases 2/3 in rat brain

The homologous regulation of receptors is mediated by G protein-coupled receptor kinases (GRKs) which phosphorylate the agonist-activated receptor. This study was designed to assess the in vivo indirect activation of adrenoceptors or 5-HT receptors by the reuptake blocker desipramine or fluoxetine on the cellular distribution of GRK 2/3 in rat brain. Immunoblot analysis (frontal cortex) with a GRK 2 antibody revealed a unique 80 kDa protein (mixed GRK 2/3) in total homogenate (H) and in membrane (P2) and cytosolic (S2) fractions. The proportion of GRK 2/3 in each fraction, relative to that of H, was: P2/H=0.11 and S2/H=0.45. Acute desipramine (noradrenaline reuptake blocker) increased in a dose- (1-30 mg/kg, i.p.) and time- (1-6 h) dependent manner the content of GRK 2/3 in the membrane (P2/H ratios increased by 37-164%). This effect vanished with a prolonged desipramine (30 mg/kg) exposure (24 h). Desipramine did not alter the content of GRK 2/3 in the cytosol (S2/H ratios). Chronic desipramine (10 mg/kg every 24 h) for 14 days did not change significantly the immunodensity of GRK 2/3 in the membrane or the cytosol. The acute administration (2 h) of fluoxetine (5-HT reuptake blocker; 3-30 mg/kg) did not induce significant changes in the content of GRK 2/3 in the membrane (P2/H ratio) or cytosol (S2/H ratio). The results indicate that the in vivo activation of adrenoceptors by desipramine is associated with a time-dependent modulation of membrane-associated GRK 2/3 (i.e. an acute increase in the kinase content which is followed by a return to the basal expression upon repeated treatment). In contrast, the acute in vivo activation of 5-HT receptors induced by fluoxetine does not result in modulation of GRK 2/3.     

盐酸氟西汀胶囊正常人体生物等效性研究

目的研究盐酸氟西汀胶囊正常人体生物等效性。方法20名健康男性志愿受试者随机交叉单剂量口服国产盐酸氟西汀胶囊(受试制剂)与进口盐酸氟西汀胶囊(参比制剂),高效液相色谱法测定血药浓度,3p97软件计算药动学参数与生物等效性。结果受试制剂与参比制剂在人体内药-时曲线呈一室模型,tmax分别为(6.45±2.91)、(5.80±2.38)h,Cmax分别为(62.59±21.21)、(65.66±38.75)ng/ml,AUC0~t分别为(3216.21±899.69)、(3219.37±867.34)(ng.h)/ml,受试制剂的相对生物利用度为(99.90±13.25)%。结论2种制剂具有生物等效性。     

阿普唑仑和氟西汀治疗顽固性功能性胃肠病的疗效比较

目的比较阿普唑仑和氟西汀治疗功能性胃肠病(FGID)的疗效,并探讨抗焦虑药和抗抑郁药在治疗FGID中的作用和地位。方法在常规疗法基础上,分别联用阿普唑仑和氟西汀治疗323例顽固性功能性消化不良(FD)和肠易激综合征(IBS)8周,并与单用常规疗法对照,评测其治疗前后消化道症状和焦虑、抑郁自评量表积分变化。结果阿普唑仑组和氟西汀组的消化道症状有效率分别为50. 9 %和55. 6 % (P=0. 552),均显著高于常规疗法的22. 4 % (P<0. 001);便秘主导型IBS消化道症状有效率三组差异无统计学意义(P=0. 990);阿普唑仑组和氟西汀组FD和腹泻主导型IBS原有精神异常患者和无精神异常患者的消化道症状有效率分别为58. 3 %和50. 8 %,差异无统计学意义(P=0. 328);阿普唑仑组和氟西汀组治疗前后焦虑自评量表(SAS)总分差值比较无统计学意义(P=0. 067),抑郁自评量表(SDS)总分差值比较则氟西汀组优于阿普唑仑组(P<0. 001)。结论阿普唑仑和氟西汀均能改善FGID的消化道症状,疗效与症状类别有关,与目前是否存在精神异常无关。     

氟西汀合用心理行为干预治疗老年期抑郁症的疗效

目的探讨氟西汀合用心理行为治疗对老年期抑郁症的疗效。方法将50例老年期抑郁症随机分成两组,进行为期6周的对照研究,出院后随访1年,分别用心理行为合并氟西汀治疗(研究组)和氟西汀治疗(对照组);采用汉密尔顿抑郁量表(HAMD)和临床疗效总评量表(CGISI)进行评定。结果研究组在治疗6周后HAMD评分(9.51±2.35)较对照组(12.87±3.48)差异有显著性(P<0.01),研究组CGISI较对照组差异有显著性(P<0.01),1年末随访时HAMD评分研究组(9.21±2.74)较对照组(13.76±4.85)差异有显著性(P<0.01)。且研究组复发率低于对照组(P<0.05)。结论氟西汀合用心理行为治疗对老年期抑郁症的疗效优于单用氟西汀,且复发率低。     

氟西汀对脑卒中后抑郁及神经功能康复的作用

目的观察氟西汀对脑卒中后抑郁及神经功能康复的疗效。方法将73例早期(<2个月)脑卒中后抑郁患者随机分为氟西汀治疗组和对照组。两组病人均予脑卒中基础治疗,同时予简单的功能训练。治疗组加用氟西汀20mg,每日1次,对照组不使用任何抗抑郁药,疗程8周。观察病人在治疗前、治疗后4周、治疗后8周Hamilton抑郁量表评分(HDRS)、Zung抑郁自评量表评分(SDS)以及生活活动量表Barthel指数(BI)的变化情况。结果治疗组治疗后4周、8周HDRS、SDS以及BI评分与治疗前比较,差异有非常显著性(P<0.01);治疗组治疗后4周、8周HDRS、SDS及BI评分,与对照组比较差异有显著性(P<0.05)。同时氟西汀无明显毒副作用,患者耐受性好,服用安全。结论氟西汀可明显改善脑卒中后抑郁患者的抑郁症状,同时还能促进神经功能康复。     

文拉法辛缓释剂与氟西汀治疗抑郁症首次发病患者的对照研究

目的：探讨文拉法辛缓释剂治疗抑郁症首次发病（以下称首发）患者的有效性及安全性。方法：采用随机、单盲对照法，将80例抑郁症首发患者分为文拉法辛组（75～225mg／d）和氟西汀组（20～40mg／d），疗程均为8周。治疗前后以汉密尔顿抑郁量表（17项，HAMD）评估疗效，记录不良反应及实验室情况。结果：实际完成80例，其中文拉法辛组40例，氟西汀组40例。治疗第2周末，文拉法辛组的HAMD总分较治疗前明显下降（t=6．47，P＜O．01）．减分率高于氟西汀组（x^2=10．05．P＜0．01）。氟西汀组HAMD总分在治疗第4周末较治疗前明显下降（忙8．097，P＜0．01）。治疗第2，4周末，文拉法辛组有效率分别为17．5％和54．8％，氟西汀组分别为2．5％和25％，组问差异均有统计学意义（x^2=12．5，P＜0．0l；x^2=18．5l，P＜0．01）。治疗第6，8周末，文拉法辛组治愈率分别为40％和62．5％，氟西汀组分别为22．5％和47．5％，组问差异均有统计学意义（x^2=6．336，P＜0．05；x^2=4．45，P＜0．05）；而两组有效率的差异无统计学意义（x^2=1．681；x^2=0．866，P＞0．05）。两组患者出现药物不良反应12例和13例（分别占30％和32．5％），差异无统计学意义（x^2=0．144，P＞0．05）。结论：文拉法辛缓释剂治疗抑郁症首发患者起效较快、安全、疗效肯定，治疗第6，8周末时治愈率高于氟西汀。