氟西汀与阿米替林治疗105例抑郁障碍病人的双盲对照试验

目的：评价国产氟西汀的抗抑郁作用及安全性。方法：采用随机、双盲对照、多中心研究，分为国产氟西汀组５７例（男性２２例，女性３５例；年龄４０±ｓ１３ａ），口服氟西汀２０ｍｇ，ｑｄ，阿米替林５７例（男性２７例，女性３０例；年龄４０±１４ａ），口服阿米替林７５ｍｇ，ｂｉｄ，疗程６ｗｋ。结果：氟西汀治疗抑郁障碍的疗效与阿米替林相当，总有效率分别为８５％及９２％（Ｐ＞０．０５）；氟西汀组的主要副作用有口干、便秘、恶心、心动过速等，但较之阿米替林程度轻且发生率低。结论：氟西汀的抗抑郁作用与阿米替林相当，副作用少，服用方便。     

氟西汀与阿米替林双盲对照治疗抑郁障碍病人16例

目的：评价国产氟西汀治疗抑郁障碍的疗效和副作用。方法：采用国产氟西汀和阿米替林双盲对照治疗１６例抑郁障碍病人。氟西汀组８例（男性３例，女性５例，年龄４５±ｓ１４ａ），用氟西汀２０ｍｇ，ｐｏ，ｑｄ。阿米替林组８例（男性３例，女性５例，年龄４４±１３ａ），用阿米替林７５ｍｇ，ｐｏ，ｂｉｄ。疗程６ｗｋ。结果：治疗后２组病人的ＨＡＭＤ，ＨＡＭＡ，ＳＤＳ评分均显著下降，显效率均为１００％，２种药物在疗效和副作用方面未有显著差异。结论：国产氟西汀是满意的新型抗抑郁剂。     

博乐欣与阿米替林治疗抑郁障碍对照观察

目的：探讨博乐欣与阿米替林对抑郁障碍的疗效及副反应。方法：对５０例抑郁障碍患者应用博乐欣（２５例）与阿米替林（２５例）进行对照治疗,疗程６周。     

西酞普兰和阿米替林治疗老年抑郁症效果比较

目的比较西酞普兰与阿米替林治疗老年抑郁症的疗效及不良反应。方法将72例符合CCMD-3诊断标准的老年抑郁症病人随机分为两组,分别采用西酞普兰和阿米替林治疗8周,采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)和副反应量表(TESS)评定疗效和不良反应。结果西酞普兰组疗效优于阿米替林组(uc=1.81,P<0.05),副作用轻于阿米替林组(t=5.01~15.91,P<0.05、0.01)。结论西酞普兰是一种既有效又安全的新型抗抑郁药,适用于老年抑郁症的治疗。     

Interstitial cystitis: bladder pain and beyond

Background: Interstitial cystitis is characterized by over 6 months of chronic pain, pressure and discomfort felt in the lower pelvis or bladder. It is often relieved with voiding, along with daytime frequency and nocturia in the absence of a urinary tract infection. Interstitial cystitis occurs primarily in females including adolescents and its diagnosis is still one of exclusion. It is now recognized as a serious medical condition associated with significant disability. Objective: The aim of this paper was to review the pathogenesis and treatment of interstitial cystitis with emphasis on new pathogenetic trends and therapeutic modalities. Methods: About 713 mostly original papers were reviewed in Medline from 1990 to August. 2008. All authors independently reviewed the literature. Large, double-blind, placebo-controlled, clinical trials were few and the medical histories of the patients used varied considerably making conclusions difficult. Promising pilot trials turned out mostly negative on follow-up. Results: Increasing evidence of co-morbid diseases, neurogenic inflammation and the effect of stress are promising as new targets for pathophysiology. No new effective treatments have emerged. Oral pentosanpolysulfate, amitriptyline, hydroxyzine and quercetin, as well as intravesical heparin/bicarbonate/lidocaine solutions, are still used with variable success. Some pilot open-label trials presented encouraging findings. Conclusion: Interstitial cystitis contributes substantially to chronic pelvic pain and to poor quality of life. Oral or intravesical administration of solutions containing sodium hyaluronate, chondroitin sulfate and quercetin to both reduce bladder inflammation and ‘replenish’ the glycosaminoglycan layer should be tried. There is a clear need for therapeutic modalities. New potential translational research areas are suggested.     

Daledalin Tosylate: A Controlled Trial in Depressive Illness

Summary

Pharmacological studies of a novel chemical - daledalin tosylate (UK 3557), an indoline compound - suggested the possibility of antidepressant activity with fewer autonomic side-effects in man. A double-blind comparison of daledalin tosylate and amitriptyline hydrochloride as a standard reference antidepressant was carried out in 28 patients with depressive illnesses. Sixteen patients received daledalin tosylate and 12 amitriptyline hydrochloride. The concept of ‘depressive illness’ and the criteria for inclusion in the study are discussed at length.

No statistically significant differences between the two drugs could be found in the Hamilton Rating Scale for Depression, the Wakefield Self-Assessment Depression Scale, global assessment of severity of illness or change in condition, side-effects check list, or the trend analysis of the laboratory results by linear regression.

It was concluded that daledalin tosylate had antidepressant effects comparable with amitriptyline but no clinical advantages over the latter.     

Ionic and cellular mechanisms underlying the development of acquired Brugada syndrome in patients treated with antidepressants

Antidepressant‐Induced Brugada Syndrome. Introduction: Tricyclic antidepressants are known to induce cardiac arrhythmias at therapeutic or supratherapeutic doses. The tricyclic antidepressant, amitriptyline, is reported to induce ST segment elevation in the right precordial electrocardiogram (ECG) leads, thus unmasking Brugada syndrome (BrS). The mechanism by which antidepressants induce the BrS phenotype and associated sudden death is not well established. Methods and Results: Action potentials (AP) were simultaneously recorded from epicardial and endocardial sites of isolated coronary‐perfused canine right ventricular wedge preparations, together with a transmural pseudo‐ECG. Amitriptyline alone (0.2 μM–1 mM) failed to induce a BrS phenotype. NS5806 (8 μM), a transient outward potassium channel current (I_to) agonist, was used to produce an outward shift of current mimicking a genetic predisposition to BrS. In the presence of NS5806, a therapeutic concentration of amitriptyline (0.2 μM) accentuated the epicardial AP notch leading to ST‐segment elevation of the ECG. All‐or‐none repolarization at some epicardial sites but not others gave rise to phase‐2‐reentry and polymorphic ventricular tachycardia (VT) in 6 of 9 preparations. Isoproterenol (100 nM) or quinidine (10 μM) reversed the effects of amitriptyline aborting phase 2 reentry and VT (4/4). Using voltage‐clamp techniques applied to isolated canine ventricular myocytes, 0.2 μM amitriptyline was shown to produce use‐dependent inhibition of sodium channel current (I_Na), without significantly affecting I_to (n = 5). Conclusions: Our data suggest that amitriptyline‐induced inhibition of I_Na unmasks the Brugada ECG phenotype and facilitates development of an arrhythmogenic substrate only in the setting of a genetic predisposition by creating repolarization heterogeneities that give rise to phase 2 reentry and VT.     

Epinephrine potentiates the analgesic and antidepressant effects of amitriptyline as a result of stimulation of the gastric mucosal afferents

Intramuscular amitriptyline in the minimum effective dose causes maximum analgesic and antidepressant effect and significant sedation in rats. Combined injection of amitriptyline with epinephrine in the threshold doses (ineffective if used alone), 1/10 and 1/30 minimum effective doses, respectively, leads to the development of the maximum analgesic and antidepressant effect, but causes no sedative side effect. This potentiation is mediated by stimulation of afferents in the gastric mucosa with epinephrine. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 144, No. 11, pp. 535–537, November, 2007