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PubMed1986

Changes in the behavioural response to a TRH analogue following chronic amitriptyline treatment and repeated electroconvulsive shock in the rat.

The arousal elicited in rats by injection into the nucleus accumbens of the thyrotrophin-releasing hormone analogue CG 3509 (orotyl-histidyl-prolineamide) was used to assess the responsiveness to thyrotrophin-releasing hormone following repeated treatment with amitriptyline or electroconvulsive shock. Fourteen day administration of amitriptyline (15 mg kg-1 i.p. twice daily) reduced the behavioural response to bilateral intra-accumbens injection of CG 3509 (2 X 2.5 micrograms). CG 3509-induced hyperactivity, recovery from pentobarbitone-induced anaesthesia and the reversal of both pentobarbitone-induced hypothermia and decreased respiration, were all significantly reduced compared to either the response of the animals prior to amitriptyline administration or that observed in rats following chronic saline administration. Repeated administration of electroconvulsive shock (5 shocks over 10 days) significantly increased CG 3509-induced hyperactivity and the degree of reversal of pentobarbitone-induced hypothermia and respiratory depression following CG 3509 administration. The results demonstrate that chronic antidepressant treatments alter the central functional responsiveness to thyrotrophin-releasing hormone. These changes are discussed with respect to the effects of antidepressant treatments on 5-hydroxytryptamine receptors and possible thyrotrophin-releasing hormone--aminergic interactions.

Amitriptyline↗
PubMed1983

A comparison of zimeldine and amitriptyline on cardiovascular effects in healthy volunteers.

The cardiovascular effects of zimeldine (200 mg) and amitriptyline (150 mg) for 6 days were compared in a study involving 10 healthy volunteers. No significant changes were found in heart rate, mean arterial blood pressure or left ventricular contractility when patients were taking zimeldine. With amitriptyline, significant changes were seen at some point during the trial period for all these parameters. No significant changes were seen in the ECGs recorded. Thus, zimeldine appears to be free of adverse effects on contractility, but amitriptyline appears to have a negative inotropic effect.

Adult↗
PubMed1984

Zimeldine versus amitriptyline in endogenous depression. A double-blind study with special reference to effects on liver function.

In a double-blind comparison of 21 inpatients with endogenous depression 225 mg zimeldine demonstrated the same degree of antidepressive efficacy as 150 mg amitriptyline after 4 weeks of treatment. Only "sleep disturbances" on the Hamilton Rating Scale for Depression (HRS) showed significant (P less than 0.05) improvement with amitriptyline. Only small differences in the frequency of side effects were seen. In the zimeldine group, increased sweating and headache were more pronounced, while the amitriptyline patients more often reported dry mouth and constipation. Body weight was not significantly changed by either treatment. In the zimeldine group, treatment had to be interrupted in three patients due to hypersensitivity reactions in the form of drug fever. Three other patients in the zimeldine group showed clinically significant elevation of liver enzymes. Hypersensitivity reactions and abnormal blood chemistry were both reversible. The adverse reactions are discussed, the cause of the occurrence remaining unknown.

Adult↗
PubMed1985

Paroxetine in the treatment of depression--a randomized comparison with amitriptyline.

Paroxetine is a new antidepressant drug with potent serotonin (5HT) uptake inhibitory properties. In this double-blind comparative study, the antidepressant effect of paroxetine and amitriptyline has been compared in 44 patients with depressive illnesses of an endogenous nature. Each drug was given for 6 weeks. The 17-item Hamilton Depression Scale was used to measure the antidepressant effect. Reported events were assessed applying a 22-item check list. Non-parametric statistical analyses were applied in the evaluation of treatment outcome for the 30 patients who completed the study. The results showed no significant differences in overall antidepressant efficacy between paroxetine and amitriptyline and that paroxetine displayed significantly fewer instances of dry mouth and orthostatic dizziness than amitriptyline. No obvious relationship was demonstrated between the plasma levels of the drugs and their clinical effects.

Adult↗
PubMed1993

A double-blind study of L-sulpiride versus amitriptyline in lithium-maintained bipolar depressives.

A double-blind group comparison study of L-sulpiride and amitriptyline was carried out in 30 bipolar outpatients on maintenance treatment with lithium suffering from a major depressive recurrence. L-sulpiride showed equivalent antidepressant activity to amitriptyline at 4 weeks using the Hamilton Rating Scale for Depression. However, the onset of action was faster in the L-sulpiride group, showing a significant improvement at 1 week in both anxiety-somatization and specific depression items, including depressed mood, feelings of guilt, work & activities and retardation. The incidence of anticholinergic side effects was significantly higher in the amitriptyline treatment group.

Ambulatory Care↗
PubMed1996

Paroxetine and amitriptyline in the treatment of depression in general practice.

A total of 144 outpatients in general practice in Denmark, aged 18-65 years and diagnosed as suffering from depression with a HAMD-17 score of 15 or more, were included in this 8-week double-blind, randomised, multicentre, controlled, parallel group comparison of paroxetine versus amitriptyline. The purpose of the study was primarily to evaluate efficacy and tolerance of treatment. In addition, focus was added on weight change and subjective well-being. The efficacy results showed equal effect of both drugs. However, paroxetine was tolerated better than amitriptyline, and this difference reached the level of significance when four non-evaluable patients were taken out of the analysis. Moreover, there was a significant weight increase in the amitriptyline group and no significant weight change in the paroxetine group. There was no difference between the groups as regards subjective well-being as measured by the VAS. In conclusion, paroxetine is an effective and well-tolerated antidepressant, and well-suited for the treatment of depression in general practice.

Adolescent↗
PubMed1997

Meta-analysis of randomized, double-blind, placebo-controlled, efficacy and safety studies of mirtazapine versus amitriptyline in major depression.

A meta-analysis was performed on efficacy and safety data from 4 randomized, double-blind, 6-week, single-center studies comparing mirtazapine (n = 194; 5-35 mg/day) with amitriptyline (n = 193, 40-280 mg/day) and placebo (n = 193) in outpatients with a DSM-III diagnosis of major depressive episode. On all the main efficacy variables both active drugs consistently produced significantly greater improvements and significantly greater percentages of responders or remitters than placebo. The meta-analysis of adverse events shows that mirtazapine was better tolerated than amitriptyline, particularly with respect to anticholinergic and cardiac adverse events. There were no differences between mirtazapine and placebo regarding the incidence of serotonergic adverse events. In conclusion, the results of this meta-analysis demonstrate that mirtazapine is as effective as amitriptyline but has a better tolerability profile.

Adolescent↗
PubMed1998

Amitriptyline vs. lorazepam in the treatment of opiate-withdrawal insomnia: a randomized double-blind study.

Benzodiazepine use in the treatment of insomnia may cause benzodiazepine dependence, especially in opiate users. The aim of this study was to investigate the sedative-hypnotic effects of amitriptyline in treating opiate-withdrawal insomnia. A total of 27 patients with opiate withdrawal were given either amitriptyline or lorazepam in a randomized double-blind trial. Sleep was assessed by means of the Sleep Evaluation Questionnaire and three insomnia items of the Hamilton Depression Rating Scale. The scores of two sleep measures showed that all aspects of sleep, except for ease of awakening from sleep, in the two treatment groups were not significantly different. In conclusion, apart from the hangover effect, amitriptyline is as effective as lorazepam in the treatment of opiate-withdrawal insomnia.

Adult↗
PubMed1999

Amitriptyline-induced release of endothelin-1 in isolated perfused and ventilated rat lungs.

We have previously shown that tricyclic antidepressants can induce vaso- and bronchoconstriction as well as oedema formation in isolated perfused lungs. This is an effect similar to that seen clinically in adult respiratory distress syndrome. In order to investigate whether endothelin can be a mediator of this reaction, isolated perfused rat lungs were exposed to 0.1 mM amitriptyline via the pulmonary circulation, perfusate was collected and endothelin-1 present in the perfusate and lavage fluids was determined by radioimmunoassay. A significant increase in perfusate concentration of endothelin-1 was noted, with the highest release seen within the first 10 min. of exposure. Histamine and thromboxane have also been proposed as mediators in induction of adult respiratory distress syndrome. However, no increased amounts of these mediators were detected in the perfusate. Experiments where lungs were exposed to exogenous endothelin-1(0.1-1 nmol), both via the perfusate and via intratracheal instillation were conducted. Similar effects as observed with amitriptyline (0.1 mM) on lung function and perfusion flow were detected. In conclusion, the detection of endothelin-1 release in our lung model proposes a role for endothelin-1 in amitriptyline-induced vaso- and bronchoconstriction and possibly in adult respiratory distress syndrome type reaction. Further studies with this model are interesting in order to elucidate mechanisms behind the complex issue of adult respiratory distress syndrome-induction.

Amitriptyline↗
PubMed1985

Repeated treatment with amitriptyline reduces immobility in the behavioural 'despair' test in rats by activating dopaminergic and beta-adrenergic mechanisms.

Seven days of treatment with amitriptyline 10 mg kg-1 day-1, reduced the immobility time in the behavioural 'despair' test in rats. 0.5, but not 0.25 mg kg-1 haloperidol significantly counteracted the reduction of immobility caused by amitriptyline. Its anti-immobility effect was reduced by 50 and 100 mg kg-1 sulpiride, another blocker of dopamine receptors, and 5 mg kg-1 (+/-)-propranolol, a beta-adrenolytic drug. Prazosin, 3 mg kg-1, an antagonist of post-synaptic alpha-adrenoceptors, had no effect. It is suggested that dopaminergic and beta-adrenoceptors mediate the anti-immobility effect of repeated amitriptyline treatment in rats.

Amitriptyline↗
PubMed1996

Regioselectivity and substrate concentration-dependency of involvement of the CYP2D subfamily in oxidative metabolism of amitriptyline and nortriptyline in rat liver microsomes.

Kinetic analysis of the metabolism of amitriptyline and nortriptyline using liver microsomes from Wister rats showed that more than one enzyme was involved in each reaction except for monophasic amitriptyline N-demethylation. The Vmax values particularly in the high-affinity sites for E-10-hydroxylation of both drugs were larger than those for Z-10-hydroxylations. Their E- and E-10-hydroxylase activities in Dark-Agouti rats, which are deficient for CYP2D1, were significantly lower than those in Wistar rats at a lower substrate concentration (5 microM). The strain difference was reduced at a higher substrate concentration (500 microM). A similar but a smaller strain difference was also observed in nortriptyline N-demethylase activity, and a pronounced sex difference (male > female) was observed in N-demethylation of both drugs in Wistar and Dark-Agouti rats. The reactions with the strain difference were inhibited concentration-dependently by sparteine, a substrate of the CYP2D subfamily, and an antibody against a CYP2D isoenzyme. The profiles of these decreased metabolic activities corresponded to that of the lower metabolic activities in Dark-Agouti rats. These results indicated that a cytochrome P450 isozyme in the CYP2D subfamily was involved in E- and Z-10-hydroxylations of amitriptyline and nortriptyline in rat liver microsomes as a major isozyme in a low substrate concentration range. It seems likely that the CYP2D enzyme contributes to nortriptyline N-demethylation.

Amitriptyline↗
PubMed1995

Randomised controlled trial comparing problem solving treatment with amitriptyline and placebo for major depression in primary care.

OBJECTIVE: To determine whether, in the treatment of major depression in primary care, a brief psychological treatment (problem solving) was (a) as effective as antidepressant drugs and more effective than placebo; (b) feasible in practice; and (c) acceptable to patients. DESIGN: Randomised controlled trial of problem solving treatment, amitriptyline plus standard clinical management, and drug placebo plus standard clinical management. Each treatment was delivered in six sessions over 12 weeks. SETTING: Primary care in Oxfordshire. SUBJECTS: 91 patients in primary care who had major depression. MAIN OUTCOME MEASURES: Observer and self reported measures of severity of depression, self reported measure of social outcome, and observer measure of psychological symptoms at six and 12 weeks; self reported measure of patient satisfaction at 12 weeks. Numbers of patients recovered at six and 12 weeks. RESULTS: At six and 12 weeks the difference in score on the Hamilton rating scale for depression between problem solving and placebo treatments was significant (5.3 (95% confidence interval 1.6 to 9.0) and 4.7 (0.4 to 9.0) respectively), but the difference between problem solving and amitriptyline was not significant (1.8 (-1.8 to 5.5) and 0.9 (-3.3 to 5.2) respectively). At 12 weeks 60% (18/30) of patients given problem solving treatment had recovered on the Hamilton scale compared with 52% (16/31) given amitriptyline and 27% (8/30) given placebo. Patients were satisfied with problem solving treatment; all patients who completed treatment (28/30) rated the treatment as helpful or very helpful. The six sessions of problem solving treatment totalled a mean therapy time of 3 1/2 hours. CONCLUSIONS: As a treatment for major depression in primary care, problem solving treatment is effective, feasible, and acceptable to patients.

Adolescent↗
PubMed1979

Cardiovascular effects of amitriptyline, mianserin, zimelidine and nomifensine in depressed patients.

The cardiac effects of amitriptyline, mianserin, zimelidine and nomifensine on the systolic time intervals (STI) and on the high speed surface ECG have been studied in depressed patients. Amitriptyline increased pre-ejection period (PEP) index and the PEP/left ventricular ejection time (LVET) ratio of the STI (P less than 0.05 and P less than 0.02). It also increased heart rate significantly (less than 0.02) and tended to prolong Q-T interval. Mianserin shortened QS2I (P less than 0.05) and LVET (P less than 0.01) and prolonged PEP/LVET ratio (P less than 0.01). Zimelidine did not affect the STI but tended to decrease heart rate and prolong the Q-T interval. Nomifensine decreased T wave height. These findings indicate that amitriptyline decreases cardiac contractility and confirm the quinidine-like action of the tricyclic antidepressants. The changes brought about by mianserin are probably due to effects on the peripheral circulation rather than a direct action on the heart.

Adult↗
PubMed1982

The effect of amitriptyline, mianserin, and viloxazine at pre- and post-junctional muscarinic receptors in guinea-pig ileal longitudinal muscle.

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.

Acetylcholine↗
PubMed1984

Serum levels and response to amitriptyline in depressed out-patients.

Serum levels of amitriptyline plus nortriptyline were measured by radioimmunoassay at 1 and 6 weeks in depressed out-patients treated with amitriptyline for 6 weeks. Serum concentrations at 6 weeks were higher in older patients. Serum levels showed no relationship to clinical response at 6 weeks, and a week inverse relationship with response at 2 weeks. Routine monitoring of serum levels appears to be of little value in depressed out-patients treated with amitriptyline.

Adult↗
PubMed1995

Comparative effects of amitriptyline and amineptine in patients affected by anxious depression.

In a double-blind, placebo-controlled study, the therapeutic efficacy of two antidepressants with different neurochemical mechanisms of action, amitriptyline and amineptine, was investigated in patients affected by anxious depression. Sixty-six patients with the primary diagnosis of major depression or bipolar affective disorder (DSM-III-R) and meeting additional operational clinical criteria such as anxiety, trepidation, restlessness, early and/or late insomnia, impulsivity, hostility, dysphoria, compulsivity, hyperperspiration, palpitation, pollakiuria and phobias were included. They were randomly assigned to three groups (n = 22) and treated either with placebo, amitriptyline (up to 100 mg/day) or amineptine (up to 200 mg/day) for 6 weeks. Patients showed better response to amitriptyline, a preferential inhibitor of serotonin reuptake, than to amineptine, a selective inhibitor of dopamine reuptake. The present results suggest that alterations in serotonergic rather than dopaminergic transmission contribute to the pathophysiology of anxious depression.

Adolescent↗
PubMed1996

Modified oral anticoagulant potency in an amitriptyline-treated patient?

We report the case of a 74-year-old female patient who received the antide-pressant amitriptyline because of a major depression. Incidence of acute lower extremity venous thrombosis required an additional oral anticoagulant therapy with phenprocoumon. During the simultaneous adjustment of both substances, the Quick value displayed great fluctuations which only disappeared after discontinuation of the amitriptyline medication. This finding is discussed as an aspect of a possible drug-drug interaction between amitriptyline and phenprocoumon.

Aged↗
PubMed1976

MHPG, amitriptyline and affective disorders. A longitudinal study.

The daily urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG) were studied longitudinally in five unipolar depressed patients. The patients were followed first during a pretreatment period, and then during a treatment period in which amitriptyline was administered. The data we have obtained suggest that: (1) there is a wide individual variability in MHPG pretreatment levels: (2) amitriptyline modifies MHPG levels in a way which seems to be related to the pretreatment MHPG; (3) amitriptyline may produce a sustained improvement in depressive symptoms, independent of the pretreatment MHPG values, and (4) the time course of modifications in MHPG excretion is shorter than the time course of improvement in depression. Some theoretical implication of these findings are discussed in terms of the catecholamine hypothesis of affective disorders.

Adult↗