Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a multicenter, placebo-controlled, clinical trial, the efficacy of Limbitrol was compared with that of its components, amitriptyline and chlordiazepoxide. All patients had a diagnosis of primary depression. Data from 279 patients were evaluated using the Hamilton depression scale, the Beck depression inventory, and physician and patient global change measures. Statistically significant differences favoring Limbitrol occurred after 1 week of treatment, and a trend in favor of Limbitrol continued throughout the remaining 3 weeks. In most efficacy comparisons, the combination was as good as, or better than, amitriptyline alone. It was superior to chlordiazepoxide alone after 2 and 4 weeks of treatment. Each component produced an independent contribution to the total therapeutic effect: the chlordiazepoxide effect was more prominent in the first 2 weeks and the amitriptyline effect in the latter 2 weeks. A trend favoring amitriptyline over chlordiazepoxide was evident by week 4. The overall incidence of side effects was comparable in both Limbitrol- and amitriptyline-treated groups. Limbitrol-treated patients exhibited more sedation, but significantly fewer Limbitrol patients discontinued treatment prematurely because of side effects.
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PMID:A placebo-controlled multicenter trial of Limbitrol versus its components (amitriptyline and chlordiazepoxide) in the symptomatic treatment of depressive illness. 10 39

One-way mixed lymphocyte cultures (MLC) were performed with peripheral blood lymphocytes of 21 patients with Crohn's disease (CD) not receiving salizylazosulphapyridine, steroids or azathioprine, seven patients with inflammatory bowel disease other than CD and ulcerative colitis, and 46 age- and sex-matched normal control subjects. The group of CD patients consisted of 11 patients with newly diagnosed, short-standing and so far untreated CD (group CD 1) and 10 patients previously treated with drugs and with mostly long-standing CD (group CD 2). Results showed that the MLC responsiveness was similar in all Crohn's disease groups, normal subjects and diseased controls. While there was no correlation between MLC responsiveness and either disease activity or disease duration when compared singly, those CD 2 patients who had highly active and/or very long-standing disease did exhibit a depressed MLC responsiveness as compared with that of normal subjects (p less than 0.001), CD 1 patients who had both inactive and short-standing disease (P less than 0.05), and diseased controls (0.1 greater than or equal to P greater than 0.05). The stimulatory capacity did not differ significantly between the CD groups and normal subjects or diseased controls; the latter, however, stimulated poorly compared with normal subjects (P less than 0.05). In accordance, an inverse relationship between the magnitude of the stimulatory capacity and the disease activity was found in the CD patients as a whole. These data suggest that there is no depression of the in vitro primary cell mediated immune response as a predisposing factor for CD or as an early event associated with the pathogenesis of CD.
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PMID:Immune status in Crohn's disease. 2. Originally unimpaired primary cell mediated immunity in vitro. 15 Mar 62

1 The effects of pentobarbitone (PB) and other sedative/hypnotic drugs have been examined in relation to gamma-aminobutyric acid (GABA) in vitro on the superfused isolated superior cervical ganglion of the rat and in vivo on single units in the brain stem of the anaesthetized rat.2 PB, and other barbiturates, depolarized the ganglion in a dose-dependent manner (threshold concentration 100-300 muM, cf. GABA depolarization threshold 1 muM). The depolarization was reduced in the presence of the selective GABA antagonist (+)-bicuculline methochloride (Bic). Other non-barbiturate sedatives e.g. chlordiazepoxide, amitriptyline, promethazine at concentrations up to 2mM produced no depolarization.3 PB, tested at concentrations up to 80 muM, produced variable effects on the dose-response curve to GABA. On most occasions a slight potentiation occurred in responses to low concentrations of GABA (below 10 muM) coupled with a depression in the responses to concentrations of GABA greater than 10 muM.4 Superfusion with PB in the presence of Bic reversed the depression in the response to GABA produced by Bic. This reversal phenomenon occurred at concentrations of PB too low to depolarize the ganglion and was dependent not only on the concentration of PB but also on that of Bic.5 The reversal potency within an homologous series of barbiturates increased with the size of the alkyl substituent (R2) at C5 on the barbiturate ring. The most potent occurred when the substituent contained 5 carbon atoms (pentobarbitone and amylobarbitone); above this, activity decreased.6 PB reversed the effects of the other GABA antagonists, tetramethylenedisulphotetramine and isopropyl bicyclophosphate and also the non-selective antagonism produced by strychnine. A concomitant reduction by strychnine of responses to the cholinomimetic, carbachol, was not reversed by PB.7 Non-barbiturate sedative/hypnotics also reversed the GABA antagonism produced by Bic. The benzodiazepines were effective at lower concentrations than PB (chlordiazepoxide threshold concentration 0.5 muM, cf. PB 5 muM), however, they only produced a partial reversal even at concentrations much higher than the maximally effective concentration of PB.8 The Bic reversal effect of chloridazepoxide (and other benzodiazepines) lasted many hours after removal from the superfusion solution. By contrast the effect of PB lasted only 15-30 min after its removal.9 Chlordiazepoxide (30 muM) applied in the absence of Bic did not affect the response to GABA but did reduce the depression produced by the subsequent application of Bic even though the chlordiazepoxide had been removed 40 min earlier.10 In the rat brain stem in vivo PB, applied iontophoretically in amounts which neither decreased the spontaneous neuronal firing rate nor affected the response to GABA or glycine, reversed the GABA antagonism induced by iontophoretic application of Bic (in all 23 neurones tested). PB also reversed the antagonism produced by strychnine of responses to glycine although this was less readily observed (5 out of 14 neurones tested).11 Iontophoretic application of other barbiturates and chlordiazepoxide also reversed the effect of Bic. Chlordiazepoxide only produced a partial reversal, as in the isolated ganglion, and no reversal could be demonstrated with flurazepam.12 Intravenous administration of thiopentone (1.3 mg/kg) pentobarbitone (0.4-5.5 mg/kg) hexobarbitone (0.4-0.8 mg/kg) and clonazepam (0.1-0.2 mg/kg) also reversed the effect of iontophoretically applied Bic. The reversal by clonazepam was of much longer duration than that produced by the barbiturates.13 It is suggested that the reversal exhibited by PB and the other hypnotics may be explained by assuming that the amino acids and their antagonists bind to the membrane at separate sites. If the reversal agent has particular affinity only for the antagonist binding site then it may displace the antagonist without affecting the receptor.
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PMID:Reversal of the action of amino acid antagonists by barbiturates and other hypnotic drugs. 20 5

Chlorodiazepoxide (CDP) produces stimulation of the locomotor activity of CD-1 and DBA/2 mice. This effect is strongly pronounced at the commencement of the testing session, and it is followed by a decline of the locomotor activity. The drugs impairing noradrenergic transmission: reserpine, clonidine and alpha-methyltyrosine, depressed or abolished the stimulatory effect of CDP; clonidine, in addition antagonized the subsequent decline of the locomotor activity in CDP-treated mice. Mice receiving reserpine subchronically (in the dose of 0.5 mg/kg daily for 3 days) displayed either motor depression or hypermotility. In approx. 50% of subchronically reserpinized mice CDP produced a strong hypermotility, lasting for at least 1 hr. It can be concluded that a noradrenergic mechanism is involved in the stimulatory effect of CDP on exploratory locomotor activity in mice, and that there exist two distinct subpopulations within the CD-1 strain, reacting differently to chronic reserpine treatment.
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PMID:Stimulatory effect of chlordiazepoxide on locomotor activity in mice: importance of noradrenergic transmission. 22 33

A questionnaire regarding medication preferences for major categories of psychiatric disorders was sent to 1,059 psychiatric drug investigators in 53 countries. 264 questionnaires were returned, of which 165 were appropriate for this survey. A total of 87 different psychotropic drugs were selected. Chlorpromazine was the medication most frequently cited in the treatment of schizophrenia. Amitriptyline and imipramine together accounted for the vast majority of medication chosen for all varieties of depression. In the treatment of mania, chlorpromazine was chosen by almost one-third of our sample, lithium by only one-fifth. Chlordiazepoxide and diazepam were equally preferred in the treatment of alcoholism. Most psychiatrists preferred not to use any psychotropic medications consistently in treating patients with organic brain syndromes. The implications of this study are discussed and compared uith similar studies in more limited geographical regions and in children.
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PMID:Use of psychotropics in the world. 62 3

1 Effects of a range of doses of cocaine and chlordiazepoxide given separately and as mixtures were determined on the spontaneous locomotor activity of mice. 2 Cocaine increased locomotor activity (walking) during 3 or 5 min trials in a dose-related manner. 3 Chlordiazepoxide had little effect on the total amount of locomotor activity except for depression at very high doses. A lower dose of chlordiazepoxide increased activity at the beginning of the trials only. 4 Mixtures containing certain doses of cocaine and chlordiazepoxide increased locomotor activity ot a much greater extent than cocaine alone. This high level of activity was manifested throughout 5 min trials. 5 This action of cocaine is similar to that of amphetamine.
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PMID:Interaction of cocaine with chlordiazepoxide assessed by motor activity in mice. 83 94

We examined the relative clinical efficacy of three commonly used antianxiety medications and a placebo as adjuncts to analgesic treatment of chronic cancer and arthritic pain. Nine patients with chronic pain, including six with malignancy and three with rheumatic diseases, were each exposed to three treatment phases with antianxiety drugs (hydroxyzine, prochlorperazine, and chlordiazepoxide) and one placebo phase in a double-blind, counter-balanced design. Each phase lasted 2 weeks, with analgesic medication given throughout. Pre- and post-phase measures of anxiety, depression, and hostility were taken, together with daily reports by the patients on pain, mood, and medication intake. None of the antianxiety drugs were significantly more effective than the placebo in reducing pain levels, daily medication usage or hostility. Chlordiazepoxide significantly reduced anxiety and depression compared with the placebo, but also produced the most side effects (e.g., drowsiness). The preliminary findings failed to support the efficacy of the three antianxiety medications as analgesic adjuncts.
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PMID:Adjunctive antianxiety agents in the management of chronic pain. 285 56

Systemic pretreatment with ketanserin, a relatively specific type-2 serotonin receptor antagonist, significantly attenuated the muscle rigidity produced in rats by the potent short-acting opiate agonist alfentanil. Following placement of subcutaneous electrodes in each animal's left gastrocnemius muscle, rigidity was assessed by analyzing root-mean-square electromyographic activity. Intraperitoneal ketanserin administration at doses of 0.63 and 2.5 mg/kg prevented the alfentanil-induced increase in electromyographic activity compared with animals pretreated with saline. Chlordiazepoxide at doses up to 10 mg/kg failed to significantly influence the rigidity produced by alfentanil. Despite the absence of rigidity, animals that received ketanserin (greater than 0.31 mg/kg i.p.) followed by alfentanil were motionless, flaccid, and less responsive to external stimuli than were animals receiving alfentanil alone. Rats that received ketanserin and alfentanil exhibited less rearing and exploratory behavior at the end of the 60-min recording period than did animals that received ketanserin alone. These results, in combination with previous work, suggest that muscle rigidity, a clinically relevant side-effect of parenteral narcotic administration, may be partly mediated via serotonergic pathways. Pretreatment with type-2 serotonin antagonists may be clinically useful in attenuating opiate-induced rigidity, although further studies will be necessary to assess the interaction of possibly enhanced CNS, cardiovascular, and respiratory depression.
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PMID:Ketanserin pretreatment reverses alfentanil-induced muscle rigidity. 311 50

We randomly assigned 425 outpatients, independently classified as primarily depressed by two trained psychiatrists, to double-blind treatment with Imipramine hydrochloride, chlordiazepoxide hydrochloride, or placebo. Those patients who remained at least moderately depressed (following a two-week placebo washout period) were treated for an additional eight weeks. An endpoint analysis of 387 patients who completed two or more weeks of medication disclosed early therapeutic advantages of chlordiazepoxide. By week 4 of treatment, however, imipramine produced more improvement than did placebo and chlordiazepoxide. By six and eight weeks a general, marked therapeutic advantage was found for imipramine relative to placebo and to chlordiazepoxide on measures of depression, anxiety, anger-hostility, interpersonal sensitivity, and global improvement. Chlordiazepoxide-treated patients generally did significantly better on sleep difficulty but significantly worse on anger-hostility and interpersonal sensitivity than did imipramine- or placebo-treated patients.
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PMID:Imipramine and chlordiazepoxide in depressive and anxiety disorders. I. Efficacy in depressed outpatients. 351 Jun 1

Chlordiazepoxide-amitriptyline (Limbitrol) has been shown to be more rapidly effective than amitriptyline alone for treating depression. A double-blind, randomized study was designed to compare the effects of Limbitrol and amitriptyline on insomnia, anxiety, and depression. The rate of improvement of symptoms was faster with Limbitrol. No differences were noted between groups in the degree or rate of improvement of the sleep laboratory parameters nor in sleep Stages 1 to 4. Percentages of rapid eye movement (REM) sleep and REM latency were similarly affected by the drugs, but REM density showed a significantly greater decrease with Limbitrol. Phasic REM factors may be crucial in the role of REM sleep and depression.
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PMID:Comparative effects of limbitrol and amitriptyline on sleep efficiency and architecture. 353 90


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