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PubMed1993

Computerised psychomotor performance testing: a comparative study of the single dose pharmacodynamics of minaprine and amitriptyline in young and elderly subjects.

The psychomotor and cardiovascular effects of minaprine 100 mg, a novel antidepressant, were compared with amitriptyline 25 mg, as a positive control, and placebo in a single dose randomised double-blind crossover trial using an automated psychomotor test battery (APT), postural sway (PS), blood pressure (BP) and pulse in nine young and nine elderly healthy subjects. Analysis of variance, taking into account baseline values, showed that continuous attention test (CAT), critical flicker fusion threshold (CFFT), decision making test (DMT) and paired word association (PWA) were significantly impaired with amitriptyline compared with minaprine and placebo. Minaprine did not differ from placebo. Amitriptyline significantly lowered supine systolic blood pressure (BP) and all treatments produced significant decreases in heart rate in young and elderly. No age effect on psychomotor performance was seen. Minaprine compared favourably with amitriptyline using the APT with the doses used. The APT is useful in the evaluation of new drugs on psychomotor performance.

Adult↗
PubMed1998

Symptom relief with amitriptyline in the irritable bowel syndrome.

Anti-depressants have been reported to be useful in the management of the Irritable Bowel syndrome. We studied the efficacy of amitriptyline for 12 weeks in a randomized double-blind placebo-controlled trial. Forty patients who met predefined criteria entered the trial. They received 25 mg amitriptyline for the first week, 50 mg for the second week and 75 mg nightly thereafter until the end of the 12th week. The drug and placebo groups were comparable in all major pretreatment variables. Amitriptyline was found to be significantly more effective than placebo in producing global improvement, increasing feelings of well-being, reducing abdominal pain and increasing satisfaction with bowel movements. Younger age and increasing extroversion predicted a better response to amitriptyline. Severity of depressive and anxiety symptoms and other personality variables did not influence outcome.

Adult↗
PubMed1992

Amitriptyline prevents N-methyl-D-aspartate (NMDA)-induced toxicity, does not prevent NMDA-induced elevations of extracellular glutamate, but augments kainate-induced elevations of glutamate.

The effect of amitriptyline on kainate- and N-methyl-D-aspartate (NMDA)-induced toxicity and release of amino acids from cerebellar granule neurons was studied. The ED50 for amitriptyline, imipramine, and nortriptyline protection against NMDA-induced toxicity was 6.9, 6.5, and 1.3 microM, respectively. None of these compounds protected against kainate-induced toxicity. Even though amitriptyline was protective against NMDA-induced toxicity, it had no effect on the NMDA-induced increase in extracellular levels of glutamate or aspartate from these cells, indicating a dissociation between NMDA receptor activation (as indicated by glutamate content elevations) and NMDA-induced toxicity. However, kainate and quisqualate treatment resulted in elevations of glutamate and taurine levels that were further augmented in the presence of 25 microM amitriptyline. These findings confirm the reports of others that tricyclic antidepressants have neuroprotective effects related to the NMDA receptor and expand on these reports by showing that even though there is protection against toxicity, the NMDA receptor is nevertheless activated, suggesting an involvement of these compounds at sites removed from the receptor. Furthermore, this is the first report showing an interaction of tricyclic antidepressants with the function of non-NMDA receptors.

Amitriptyline↗
PubMed1994

A comparative study of amitriptyline and fluvoxamine in migraine prophylaxis.

Current treatment of migraine either abortive or prophylactic is often unsatisfactory. Prophylactic treatment of severe migraine may reduce attack frequency, and current therapy centers on beta-blockers, serotonin (5-HT) reuptake blockers and 5-HT2 receptor antagonists. The author compared the efficacy and safety of amitriptyline and fluvoxamine among migraine patients (24F, 8M vs. 23F, 9M) in a double blind study. The efficacy of amitriptyline has already been established by earlier clinical studies. The other investigated drug, fluvoxamine, has a more selective 5-HT reuptake blocking property than amitriptyline. In this study, amitriptyline significantly reduced the number of headache attacks, but it caused severe drowsiness in many migraineurs. The fluvoxamine also favorably influenced on the number of headache attacks and caused only slight side effects. These findings suggest, that fluvoxamine may be an alternative drug in migraine prophylaxis, however, further studies should be performed with more subjects.

Adult↗
PubMedDate not supplied

Antimalarial properties of imipramine and amitriptyline.

Dietary riboflavin deficiency is known to diminish malarial parasitemia. In this study, we determined whether imipramine and amitriptyline, drugs which inhibit riboflavin metabolism, have antimalarial efficacy. In addition, we evaluated whether these drugs, like other antimalarial agents, increase the hemolytic response to ferriprotoporphyrin IX (FP). The growth of Plasmodium falciparum (FCR3) in the absence and presence of these drugs (10 to 75 microM) was measured by determining (3H)hypoxanthine uptake by intra-erythrocytic parasites for 48 h in RPMI 1640 medium. The uptake of (3H)hypoxanthine was significantly reduced in a dose-dependent manner by both imipramine and amitriptyline. The IC50 values of imipramine and amitriptyline at 48 h were 56 and 45 microM, respectively. Both drugs enhanced hemolysis induced by FP (10 or 20 microM). No hemolysis by these drugs was detected in the absence of FP. It is concluded that the tricyclic antidepressants, imipramine and amitriptyline, possess substantial antimalarial properties.

Amitriptyline↗
PubMed1978

A clinical trial comparing sustained release amitryptyline (Saroten Retard) and conventional amitriptyline tablets (Saroten) in endogenously depressed patients with simultaneous determination of serum levels of amitryptyline and nortriptyline.

The clinical effect of a sustained release preparation of amitriptyline has been compared with that of conventional amitriptyline tablets in a double-blind cross-over study with 24 patients suffering from endogenous depression. The sustained release preparation was given in a single evening dose (9 p.m.) of two thirds the total daily dose of conventional tablets, which was given in a three times-a-day regimen (8 a.m., 12 a.m. and 9 p.m.). Serum concentrations of amitriptyline and its active metabolite, nortriptyline, were determined. No difference was found between the two preparations as regards either clinical effect or side effects. No correlation could be shown between the clinical effects and the serum concentrations of amitriptyline and nortriptyline.

Adolescent↗
PubMed1979

Amoxapine versus amitriptyline in endogenous depression. A double-blind study.

A new antidepressant, amoxapine, which is a dibenzoxazepine deprivative, was compared with amitriptyline in a randomised double-blind trial. Forty-eight patients were included and 41 completed a 4-week treatment. Most of the patients were maintained on 150 mg daily. Assessments were made by the Hamilton Psychiatric Rating Scale for Depression (HAM-D), Nurses' Observation Scale for Inpatient Evaluation (NOSIE), Clinical Global Impression (CGI) scale and Patient's Self-Evaluation. The total HAM-D score was considerably reduced in the majority of the patients. Amitriptyline was the most effective with regard to symptoms included in the factor Sleep Disturbances and-secondary maybe-towards some items included in the factor Somatization. For the remaining items,including the items of the factors Anxiety/Depression and Apathy, the last score was lower in the amoxapine group than in those treated with amitriptyline. Among the unipolar cases the amoxapine treated patients were more satisfied with regard to efficacy (P = 6.3%). The frequency of side effects such as tremor and dizziness was considerably lower in the amoxapine group. In total, the side effects lasted longer in the amitriptyline group. We conclude that amoxapine seems to be an effective antidepressant with a low frequency of side effects.

Adult↗
PubMed1981

A double blind comparison of zimelidine and amitriptyline in endogenous depression.

In a randomized double-blind group comparison study of 40 patients with endogenous depression zimelidine appeared to be as effective an antidepressant as amitriptyline at 4 and 6 weeks using the Hamilton Rating Scale (HRS) and the Montgomery and Asberg Depression Rating Scale (MADRS). At 2 weeks there was a significantly better response (P less than 0.05) on zimelidine compared to amitriptyline on the clinician's global scale and 4 out of 10 items on the MADRS suggesting an early onset of action. A significant better response to zimelidine was seen on the item somatic anxiety (HRS) while the effect on sleep and appetite was better in the amitriptyline group. There were significantly more side effects, raw and corrected, in the amitriptyline-treated group. High steady state plasma concentrations of norzimelidine (greater than 800 nmol/l) which were significantly correlated with age (r = 0.8) were associated with a significantly poorer response suggesting that a lower dose than 200 mg in older patients may be appropriate.

Adult↗
PubMed1981

Comparison of the cardiovascular effects of amitriptyline and zimelidine using thoracic impedance cardiography.

Twelve depressed patients were allocated to amitriptyline (7 days 75 mg nocte, increasing to 150 mg nocte) or zimelidine (100 mg nocte increasing to 200 mg nocte) in a randomized double-blind design. Cardiovascular assessment was made at pre-drug, 7 and 14 days using thoracic impedance cardiography, a non-invasive technique for measurement of both cardiac output (CO) and systolic time intervals. Neither drug significantly changed systolic time intervals. Amitriptyline 75 mg significantly reduced stroke volume (SV) (sitting P less than 0.02, standing P less than 0.01) with a similar trend at 150 mg. Zimelidine tended to increase SV. Heart rate (HR) was increased by amitriptyline 75 mg (P less than 0.02) but zimelidine induced no consistent changes in HR. Amitriptyline 75 mg in the standing data reduced CO (P less than 0.005). In contrast zimelidine 100 mg increased sitting CO (P less than 0.05) and this trend was seen at 200 mg in both sitting and standing data. The results suggest that zimelidine has low cardiotoxicity and may have a role in the treatment of depressed patients with cardiovascular disease.

Amitriptyline↗
PubMed1981

Zimelidine and amitriptyline in the treatment of depressive illness in general practice.

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.

Adult↗
PubMed1983

Comparison between zimeldine and amitriptyline of efficacy and adverse symptoms--a combined analysis of four British clinical trials in depression.

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.

Adult↗
PubMed1983

Zimeldine tolerability in comparison to amitriptyline and placebo: findings from a multicentre trial.

Zimeldine tolerability was compared to amitriptyline and placebo in a large multicentre study performed at three clinical research units in the U.S.A. Prior to a placebo washout period of 3-7 days, patients were randomly assigned to zimeldine, a potent and selective 5-HT reuptake blocker, amitriptyline or placebo. Dosage range was 75-300 mg/day for active medications, and the scheduled treatment period was 4 weeks. The side-effects were recorded by using a Treatment Emergent Symptom Scale (TESS). Vital signs were monitored and laboratory investigations, including chemistry and drug plasma levels, were performed. Two hundred and sixty-three patients were included in the safety evaluation. Side-effects, particularly anticholinergic effects but also drowsiness and cardiovascular effects, were much less pronounced in the zimeldine group compared to the amitriptyline group. Only marginal differences in side-effects were reported between zimeldine and placebo. Significantly more patients receiving amitriptyline were withdrawn from treatment as a result of adverse effects. Thus, zimeldine appears to be an effective antidepressant with marked advantages with regard to tolerability. It is therefore an important new contribution to the treatment of depressive disorders.

Adult↗
PubMed1983

The effects of zimeldine and amitriptyline on car driving and psychomotor performance.

The development of an objective measure of car driving performance, brake reaction time (BRT), is described, and the effects of amitriptyline and zimeldine on this measure are compared in a placebo-controlled, acute, single dose, volunteer study. The effects of treatment on laboratory tests of critical flicker fusion (CFF) threshold, choice reaction time (CRT) and tracking accuracy and on self-assessments of sedation are also examined. At 2 hours post-treatment, amitriptyline produced a significant increase in brake reaction time when compared to both placebo and zimeldine. At 4 hours post-treatment, a significant reduction in "tracking accuracy" and a significant increase in CRT was observed after treatment with amitriptyline, while no such effects were seen with zimeldine. Measures of CFF threshold and self-ratings of sedation also revealed that amitriptyline produced a significant degree of sedation at 4 hours when compared to zimeldine and placebo. In contrast, zimeldine produced elevated CFF threshold, but did not affect self-ratings of sedation.

Adult↗
PubMed1990

Moclobemide versus amitriptyline in the treatment of depression: two small double-blind multicentre studies in Belgium.

Moclobemide was compared with amitriptyline for antidepressant efficacy, safety and tolerance. Two studies were conducted, both over at least 4 weeks; in the first, 8 patients were given moclobemide in doses ranging from 300 to 328 mg, and 9 patients amitriptyline in doses of 75 to 96 mg; in the second, the numbers were 13 on moclobemide and 14 on amitriptyline, and the mean doses were 294-408 mg and 95-129 mg respectively. Both studies showed the 2 treatments to be equally effective, and there were no significant differences at any point. Moclobemide appeared slightly more effective and slightly better tolerated than amitriptyline, but the numbers were too small for any valid conclusion.

Adult↗
PubMed1980

Effects of amitriptyline and clomipramine in the isolated, perfused rabbit heart.

The cardiac effects of supratherapeutic concentrations of two tricyclic antidepressants were studied in isolated rabbit hearts, which were perfused with a modified Krebs-Henseleit solution containing 0.25 or 0.50 micrograms ml-1 of amitriptyline or 0.28 micrograms mg-1 of clomipramine. The following parameters were continuously recorded:heart rate, amplitude and rate of contraction, coronary flow rate, myocardial oxygen consumption and ECG. The lowest concentration of amitriptyline caused a time correlated decrease (20%) in the frequency of spontaneous beating and a pronounced decrease in the amplitude (62%) and rate of cardiac contraction (58%). Maximum increases of the PQ-interval of about 46% and of the QRS-complex of about 100% were observed. At the higher amitriptyline concentration these effect further increased. Clomipramine 0.28 micrograms ml-1 also had a very pronounced and time correlated negative inotropic effect, but the effects upon the conduction velocities were substantially lesser than those produced by the equimilar concentration of amitriptyline. The compounds caused only insignificant changes in coronary flow. The oxygen consumption did not decrease in proportion to the decrease in contractility, as an expression of decreased myocardial efficiency. The effects of the drugs are discussed in relation to theri myocardial accumulation pharmacokinetics and influence upon the membraneous sodium and calcium flux and intracellular metabolism.

Amitriptyline↗
PubMed1978

The use of 13C-nmr spectroscopy for the detection and identification of metabolites of carbon-13 labelled amitriptyline.

The antidepressant drug amitriptyline and two of its metabolites, nortriptyline and desmethylnortriptyline, each containing two 13C atoms, have been used to determine the sensitivity and selectivity of 13C-nmr spectroscopy for the detection of unchanged amitriptyline and N-desmethyl metabolites in the urine of animals dosed orally with the labelled drug. The resonance signals from the 13C atoms detected in the 13C-nmr spectrum of entire extract from a control 12 h rat urine sample to which 1 mg of each labelled compound had been added were easily detected, using an instrument accumulation time of 1 h. The 13C-nmr spectrum of an extract of hydrolysed urine from a dog that had received an oral dose of [13C2]amitriptyline (30mg) exhibited signals that could be assigned to metabolites resulting from N-dealkylation and N-oxidation, as well as those bearing the intact amitriptyline side-chain. These assignments were confirmed by analysis of the same extract by g.c.--ms and h.p.l.c.

Amitriptyline↗
PubMed1998

Amitriptyline and clomipramine increase the concentration of administered L-tryptophan in the rat brain.

The tricyclic antidepressant amitriptyline has been shown to reduce concentrations of large neutral amino acids (LNAA) in rat plasma. Compounds with that property might interact with such amino acids used as therapeutic agents with a central site of action by causing a change in the relationship between the administered LNAA and its endogenous LNAA competitors for carrier-mediated transport through the blood-brain barrier into the brain. This study was performed to investigate if the antidepressant agents amitriptyline and clomipramine could, by such a mechanism, increase brain concentrations of administered tryptophan. Intraperitoneal administration of L-tryptophan alone (100 mg kg-1) resulted in an increase in the concentration of tryptophan in the rat brain from 14 +/- 0.7 to 100 +/- 4.3 nmol g-1 compared with rats given saline only. When rats were given tryptophan with amitriptyline (25 mg kg-1, i.p.) or clomipramine (25 mg kg-1, i.p.) brain concentrations of tryptophan were increased even further, to 150 +/- 4.5 and 157 +/- 10.2 nmol g-1, respectively. Administration of L-tryptophan alone resulted in an increase in the rat plasma tryptophan ratio [(concentration of tryptophan)/(total concentration of LNAAs)] from 0.14 +/- 0.003 to 0.42 +/- 0.011 compared with rats given saline only. When rats were given tryptophan with amitriptyline or clomipramine the plasma tryptophan ratios were increased even further to 0.52 +/- 0.017 and 0.54 +/- 0.025, respectively. All these effects were statistically significant (P < 0.001). These findings support the hypothesis that tricyclic antidepressants could interact with administered tryptophan by changing the relationship in plasma between tryptophan and its endogenous LNAA competitors for transport into the brain, resulting in higher concentrations of tryptophan in the brain. It is possible that this could be the mechanism of the previously reported finding that clomipramine and tryptophan potentiate each other in the treatment of depression.

Amino Acids↗
PubMed2006

Use-dependent block by lidocaine but not amitriptyline is more pronounced in tetrodotoxin (TTX)-Resistant Nav1.8 than in TTX-sensitive Na+ channels.

The excitability of sensory neurons depends on the expression of various voltage-gated Na+ channel isoforms. The tetrodotoxin-resistant (TTXr) Na+ channel Na(v)1.8 accounts for the electroresponsiveness of nociceptive neurons and contributes to inflammatory and neuropathic pain. Na+ channel blockers are clinically employed for chronic pain management, but side effects limit their use. There is conflicting information whether their potency to block tetrodotoxin-sensitive (TTXs) and TTXr Na+ channels differs. We analyzed the action of lidocaine and amitriptyline on TTXr Na(v)1.8 heterologously expressed in ND7/23 cells in comparison with TTXs Na+ channels endogenously expressed in ND7/23 cells. TTXr Na(v)1.8 and TTXs currents were investigated under whole-cell voltage-clamp. At a holding potential of -80 mV, lidocaine was 5-fold and amitriptyline 8-fold more potent to tonically block TTXs than Na(v)1.8 currents. This was due to a higher percentage of TTXs channels residing in the inactivated, high-affinity state at this potential. Tonic block of either resting or inactivated channels by lidocaine or amitriptyline revealed little differences between TTXs and Na(v)1.8 channels. Use-dependent block by amitriptyline was similar in TTXs and Na(v)1.8 channels. Surprisingly, use-dependent block by lidocaine was more pronounced in Na(v)1.8 than in TTXs channels. This result was confirmed in dorsal root ganglion neurons and is associated with the greater tendency of Na(v)1.8 to enter a slow inactivated state. Our data suggest that lidocaine could selectively block Na(v)1.8-mediated action potential firing. It is conceivable that the expression pattern of Na+ channels in sensory neurons might influence the efficiency of Na+ channel blockers used for chronic pain management.

Amitriptyline↗