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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The similarities and differences in the clinical response and incidence of adverse symptoms between zimeldine and amitriptyline have been evaluated by use of a combined analysis of four double-blind clinical trials in depression. In total, 197 patients were included in this series of studies. The efficacy of the drugs was assessed using the Hamilton Rating Scale for Depression (HAM-D). Reports of adverse symptoms were actively elicited by use of a check-list of symptoms and rated for severity. The overall clinical efficacy of the two drugs was shown to be equivalent with a high degree of statistical confidence. However, there exist differences in the profile of action. Amitriptyline has a significant advantage in insomnia problems. In spite of this zimeldine was shown to be at least as effective as amitriptyline in reducing anxiety. Amitriptyline is associated with significantly more anticholinergic side-effects, whereas headache is more disturbing during zimeldine treatment. The combination of several independent trials based on similar protocols can be a useful tool to increase the statistical reliability of conclusions relative to that which can be achieved in standard sized, individual studies in depression.
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PMID:Comparison between zimeldine and amitriptyline of efficacy and adverse symptoms--a combined analysis of four British clinical trials in depression. 623 Aug 96

The antimuscarinic activity of amitriptyline, desipramine, iprindole, mianserin and viloxazine on prejunctional sympathetic nerve endings were compared in the isolated rabbit ear artery. In the presence of cocaine (10 micro M) and yohimbine (1 micro M), amitriptyline (0.5-1 micro M), desipramine (1-3 micro M) and iprindole (5-10 micro M) produced parallel rightward shifts of the concentration-response curve for the inhibitory effect of carbachol (CCh) on responses to electrical stimulation of the preparation at 3 Hz. Mianserin (3 micro M) produced some inhibition but altered the slope of the concentration-responses curve to CCh while viloxazine (less than or equal to 10 micro M) produced no inhibition. The depression of tritium efflux by CCh from arteries preincubated in 3H-noradrenaline was inhibited significantly (P less than 0.05) by amitriptyline (0.1 micro M) and desipramine (1 micro M) and not by iprindole (17 micro M), mianserin (3 micro M) or viloxazine (10 micro M). Amitriptyline was 10-fold more active than desipramine and at least 30-fold more active than the other antidepressants as a muscarine receptor blocking drug in this preparation. Thus, mianserin, viloxazine and iprindole exhibit much weaker antimuscarinic activity relative to amitriptyline on prejunctional muscarine receptors on sympathetic nerve endings compared with that observed by others for excitatory muscarine receptors in sympathetic ganglia. The findings support an earlier suggest that these receptors differ.
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PMID:The effect of some antidepressants on prejunctional muscarinic receptors on the sympathetic nerves of the isolated rabbit ear artery. 628 34

Depressive patients seen at hospital clinics are likely to be unrepresentative in terms of treatment response. In this study patients were always seen at their general practitioners' surgeries for assessment by specialists after selection as being in need of antidepressant treatment. The Research Diagnostic Criteria for major or minor depressive illness and a Hamilton Depression (Ham-D) score of at least 10 were required for inclusion, using the Present State Examination as a basis for interview. Patients were seen at weekly intervals, alternatively by practitioner and assessor for further Ham-D ratings, completion of the Kellner Sheffield Self-Rating test (KSSRT), event record and side effect checklist. Patients were randomly and blindly allocated to either zimelidine or amitriptyline dispensed identically at dosages of 100 mg and 75 mg at night, rising to 200 mg and 150 mg after two weeks. At four weeks there was no significant difference between the improvement found with zimelidine and amitriptyline or either the Ham-D or the KSSRT. Amitriptyline patients tended to gain and zimelidine patients to lose weight; difference significant. Other amitriptyline side effects were not found in those taking zimelidine, the latter tending to suffer diarrhoea. Preliminary analysis shows no relationship between clinical response and plasma level of either compound.
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PMID:Zimelidine and amitriptyline in the treatment of depressive illness in general practice. 645 5

Amitriptyline-perphenazine (100/8-150/12 mg/day) and doxepin (100-150 mg/day) were compared for clinical efficacy and safety in a sample of 130 nonpsychotic depressed outpatients. Maximum study duration was 4 weeks; 19 amitriptyline-perphenazine and 29 doxepin patients completed less than or equal to 3 weeks of treatment and 45 amitriptyline-perphenazine and 37 doxepin patients completed 4 weeks of treatment. Patients in both groups showed significant improvement in depression, but amitriptyline-perphenazine produced greater improvement than doxepin on several measures of depressive symptomatology. The incidence of anticholinergic and sedative side effects was higher in the amitriptyline-perphenazine treated group.
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PMID:Amitriptyline-perphenazine and doxepin in depressed outpatients: a controlled double-blind study. 674 26

Noradrenaline levels and platelet and free serotonin concentrations were studied in depressed women in-patients (n=78) before and during amitriptyline (n=41) or lithium treatment (n=37). Pronounced monthly differences in platelet serotonin level have been shown in these subjects before treatment. In all clinical subgroups (neurotic, involutional, manic-depressive patients) a significant fall in platelet serotonin level was observed with amitriptyline medication while an increase was noted with lithium. No significant correlations between serotonin concentrations and clinical outcome were found. Amitriptyline treatment also produced a decrease in peripheral noradrenaline concentration in all subgroups, while an increase was observed with lithium. Some correlations between noradrenaline level and degree of depression were noted in patients treated with amitriptyline or lithium. A more extended analysis of blood amine levels could supply meaningful information on the peripheral action of antidepressive drugs on noradrenaline and serotonin concentrations in depression.
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PMID:Blood noradrenaline and 5-HT levels in depressed women during amitriptyline or lithium treatment. 681 45

The perceived intensity of a stimulus may be magnified during depression. Stimulus intensity control can be studied by means of cortical evoked potentials. In a study of 33 depressives, cortical evoked potentials were greater during depression than on recovery. The effect of doxepin on the amplitudes of evoked potentials of depressives was compared with that of amitriptyline. Doxepin reduced amplitudes. Amitriptyline had a similar, but non-significant effect.
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PMID:Stimulus intensity control in depression: a study of the comparative effect of doxepin and amitriptyline on cortical evoked potentials. 693 66

Rats working on a food-reinforced operant schedule and exhibiting behavioral depression following administration of D,L-5-hydroxytryptophan (5-HTP) were pretreated with one of three drugs: methysergide, fluoxetine, or amitriptyline. The former two drugs were used to establish a basis for distinguishing between pre- and postsynaptic events. We found that methysergide, a known postsynaptic blocker of serotonin, almost completely abolished the depressive effect of 5-HTP, whereas fluoxetine, a known specific uptake blocker of serotonin, potentiated the depressive effect of the 5-hydroxytryptamine (5-HT) precursor. Amitriptyline, one of the commonly prescribed antidepressive drugs, reduced the behavioral depression following 5-HTP by approximately 50%. These data indicate that amitriptyline can act as an antagonist of 5-HT at the postsynaptic receptor. The results of this study, as well as those recently reported from CNS membrane binding studies, suggest that the therapeutic effects of some antidepressive drugs may be explained by their postsynaptic rather than presynaptic properties at central serotonergic receptors. Thus, these studies support the hypothesis that some types of human depression may be primarily due to an excess of free 5-HT acting at postsynaptic receptors.
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PMID:Pre- and postsynaptic serotonergic manipulations in an animal model of depression. 696 15

The ability of antidepressant drugs, electroconvulsive treatment (ECT), or lithium chloride (LiCl), to modify prolactin secretion in the rat was studied. Chlorimipramine, citalopram, fluoxetine, imipramine and zimelidine potentiated the low dose 5-hydroxytryptophan (5-HTP)-induced increase in prolactin secretion, suggesting inhibition of serotonin (5-HT) uptake by these drugs. Amitriptyline, doxepin, iprindole, mianserin and trazadone inhibited the prolactin stimulating effects of high doses of 5-HTP and quipazine, suggesting that these drugs have 5-HT receptor blocking properties. Tandamine inhibited only 5-HTP-induced increase in prolactin secretion. Chronic administration of imipramine, potentiated the effect of low dose 5-HTP significantly more than an acute dose. Amitriptyline, produced similar inhibition of the 5-HTP-induced increase in prolactin secretion after both acute and chronic administration. The ability of bupropion and mazindol to inhibit alpha-methylparatyrosine-induced prolactin secretion, and of nomifensine to inhibit reserpine-induced prolactin secretion, is consistent with other evidence that these agents are indirect dopamine (DA) agonists. Desipramine, acutely, had no effect on any of the above paradigms but after chronic administration, potentiated the effect of low dose 5-HTP on prolactin secretion. Nortriptyline had no effect on prolactin secretion after acute or chronic treatment. ECT for 10 days did not affect the ability of a 5-HT agonist or d-amphetamine to modify prolactin secretion. However, chronic, but not acute, treatment with LiCl markedly enhanced the prolactin response to 5-HT agonists and reserpine while shifting the dose response curve for d-amphetamine and apomorphine to the right. These results are discussed in light of current theories of the role of 5-HT and DA in depression.
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PMID:Effect of antidepressants, lithium and electroconvulsive treatment on rat serum prolactin levels. 697 60

The antimuscarinic activity of amitriptyline, mianserin, and viloxazine was compared with atropine in guinea-pig ileal longitudinal muscle. The pA2 values obtained using carbachol (CCh) as agonist were as follows: atropine, 9.55; amitriptyline, 7.50; mianserin, 6.40; and viloxazine, 4.91. Responses to transmural electrical stimulation (1-50 Hz) were more resistant than those produced by CCh to inhibition by atropine and the antidepressants. This did not appear to be due to a selective inhibition of prejunctional inhibitory muscarinic receptors, as a pA2 of 8.73 was obtained with atropine for the depression of oxotremorine-induced inhibition of acetylcholine (ACh) output. Amitriptyline (10 micrometers) caused a 2.4-fold increase in ACh output and was 200-fold weaker than atropine at doubling ACh output in the longitudinal muscle stimulated at 0.3 Hz. Mianserin (10 micrometers) and viloxazine (1-10 micrometers) did not significantly affect ACh output. It is suggested that the antidepressants exhibits a greater affinity for the postjunctional muscarinic receptors in the guinea-pig ileal longitudinal muscle.
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PMID:The effect of amitriptyline, mianserin, and viloxazine at pre- and post-junctional muscarinic receptors in guinea-pig ileal longitudinal muscle. 708 67

Factors that contribute to the lethality of amitriptyline overdosage were studied in cats. Amitriptyline (50 mg/kg) given i.p. to unanesthetized cats produced convulsions in all of the animals and death in five of six animals; pretreatment with diazepam (5 mg/kg) protected against the convulsions and death. Respiratory depression contributed to the mortality when amitriptyline was given i.v. in cats anesthetized with pentobarbital as indicated by the finding that artificial respiration delayed the time of death induced by a continuous i.v. infusion of the drug. The i.v. infusion of amitriptyline in pentobarbitalized cats under artificial respiration produced death due to cardiovascular collapse. The latter was characterized by hypotension, bradycardia, depression of myocardial contractile force, atrioventricular block, intraventricular conduction delay and cardiac arrhythmias. These effects appear to be due to a direct membrane (quindine-like) cardiotoxic action of amitriptyline. Dopamine and dobutamine were effective in protecting the animals against the acute cardiovascular collapse induced by amitriptyline. The protection was associated with a diminution of the hypotension, the negative inotropic and chronotropic actions and the incidence of atrioventricular block produced by the tricyclic antidepressant drug. The results suggest that the positive chronotropic, inotropic and dromotropic actions of the amines may all be contributory factors in their protection action. Isoproterenol and norepinephrine were less effective than the other two amines.
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PMID:Protective action of diazepam and of sympathomimetic amines against amitryptyline-induced toxicity. 709 63


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