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PubMed1982

High-pressure liquid chromatographic determination of amitriptyline and its major metabolites in human whole blood.

A sensitive, specific, high-pressure liquid chromatographic method using an internal standard was developed for the determination of amitriptyline and its major metabolites in whole blood. Analysis was carried out on a microparticulate silica column with a mobile phase consisting of acetonitrile-methanol-aqueous ammonium hydroxide (93:7:0.4). Linear calibration curves ranging to 250 ng/ml were obtained for all compounds using UV absorbance detection at 220 nm. The lower limit of detection was 2 ng/ml for amitriptyline and 10-hydroxyamitriptyline, and 6 and 16 ng/ml for nortriptyline and its 10-hydroxylated metabolite, respectively. Human whole blood samples collected after single intravenous and single oral doses can be analyzed using this procedure.

Amitriptyline↗
PubMed1985

Inhibition of the retrograde axonal transport of acetylcholinesterase by the anti-calmodulin agents amitriptyline and desipramine.

The possible involvement of calmodulin in mediating the calcium requirement for retrograde axonal transport of acetylcholinesterase was studied in vitro in bullfrog spinal nerves, with the use of the calmodulin inhibitors amitriptyline and desipramine. When nerves were preincubated with 0.2 mM amitriptyline or desipramine for 5 h, and were then ligated and incubated for an additional 17-18 h in drug-containing medium, the accumulation of acetylcholinesterase distal to the ligature was significantly reduced as compared to contralateral control nerves maintained in drug-free medium. The identical degree of transport inhibition observed for both drugs is consistent with their similar anti-calmodulin activity.

Acetylcholinesterase↗
PubMed1984

Incidence and potentiation of external and internal fetal anomalies resulting from chlordiazepoxide and amitriptyline alone and in combination.

The teratogenic potential of a combination of chlordiazepoxide (Cdz) and amitriptyline (Amt) was examined with regard to both internal and external anomalies. Timed pregnant golden hamsters were given a single intraperitoneal injection on day 8 of gestation of one of the following: chlordiazepoxide hydrochloride (28.5 mg/kg), amitriptyline hydrochloride (70.3 mg/kg), Cdz-Amt combination (28.5 mg/kg Cdz + 70.3 mg/kg Amt, in order to retain the 1:2.5 dose ratio utilized in a clinically-used preparation of these agents), or saline vehicle (control). Fetuses were recovered on gestation day 15 following maternal sacrifice. Cranial malformations were analyzed in Bouin's-fixed fetuses by making 1-mm coronal sections through each head, whereas visceral anomalies were examined following general dissection of each body. Amt alone produced a significant (P less than 0.05) incidence of bent tail and encephalocele, whereas Cdz significantly (P less than 0.05) altered the male:female ratio of surviving fetuses when compared with saline-injected controls. The Cdz-Amt combination caused significant increases in cranial malformations, open eye, bent tail, abnormal lung, and urogenital anomalies. The teratogenic effects of potentiation between the components of this combination are discussed in terms of external and internal malformations.

Abnormalities, Drug-Induced↗
PubMed1996

The opposite effects of amitriptyline on noradrenaline- and methoxamine-evoked venoconstriction in man.

The effects of a single oral dose (100 mg) of amitriptyline on noradrenaline- and methoxamine-evoked venoconstriction were compared, using the dorsal hand vein compliance technique, in 8 healthy male volunteers. Both noradrenaline and methoxamine produced dose-dependent venoconstriction; the geometric mean ED50 for noradrenaline was 4.15 ng min-1 and for methoxamine was 1143.54 ng min-1; the potency ratio (noradrenaline/methoxamine) was 277. Amitriptyline shifted the dose-response curve for noradrenaline to the left (ANOVA: P < 0.025; dose-ratio: 0.38) consistent with potentiation, and the dose-response curve for methoxamine to the right (ANOVA: P < 0.025; dose ratio: 2.72) consistent with antagonism. The potentiation is likely to be due to noradrenaline uptake blockade, whereas the antagonism is likely to reflect the blockade of post-junctional alpha 1-adrenoceptors.

Adolescent↗
PubMed1988

Experimental comparison between the effect of standardized trazodone-amitriptyline and placebo treatment in vitalized depressive patients.

We are performing a double-blind trial with inward psychiatric patients. The indication for our psychotropic or psychotherapeutic intervention is mainly severe depression (= major depressive disorders DSM III). For a 3-week trial course trazodone (400 mg daily), amitriptyline (150 mg/die) or placebo capsules were given at random. All patients received the same type of cognitive behaviour therapy. The test battery consists of CGI, BPRS, HAMD, HAMA and AMDP; adverse drug reactions are documented as "free reports" (= freier Nebenwirkungsbericht). The interim results (until March 1987) will be presented. Our investigation indicates that it is probable that the trazodone treatment we used is equivalent to corresponding amitriptyline treatment.

Adult↗
PubMed1988

Trazodone for deafferentation pain. Comparison with amitriptyline.

We report a clinical multicentre experience with antidepressant agents (trazodone and amitriptyline) in the treatment of chronic pain due to deafferentation. Forty five patients were admitted to the study; most of them with oncological peripheral nerve lesions. Almost all of them were already being treated with NSAID in association with weak or strong opioids. A random double blind study was performed: 23 patients were treated with trazodone, 22 with amitriptyline. In the assessment of results, pain intensity, hours of sleep, hours standing and lying, side effects, mood, anxiety and weakness were all taken into consideration. The therapeutic analgesic efficacy of the two drugs proved to be similar.

Adult↗
PubMed1988

Antidepressive effect of amitriptyline treatment with plasma drug levels controlled within three different ranges.

Seventy-four depressed patients were treated with amitriptyline for 4-6 weeks. Their doses were individually adjusted to maintain the sum of the plasma levels of amitriptyline (AT) and nortriptyline (NT) within one of three different ranges, randomly allocated. Allowance was made for individual plasma binding of the drugs. In the 50 patients between 25 and 65 years of age, the antidepressive response at low plasma drug levels was somewhat poorer than at medium or high levels, which were equally effective. In this age group an association was found between outcome and the individual rate of AT metabolism, expressed as "reciprocal clearance" (RC), the steady-state plasma concentration of AT plus NT divided by the daily AT dose. Good antidepressive outcome was associated with high RC. The implications of these findings for patient treatment and for the interpretation of other studies are discussed. The 18 patients between 65 and 80 years of age showed no significant differences between the effectiveness of treatment at different plasma drug levels, and no significant associations between outcome and RC.

Aged↗
PubMed1984

Inotropic effect of prenalterol in amitriptyline poisoning.

A case of severe amitriptyline poisoning with grade IV coma, seizures, bradycardia and hypotension who did not respond to dopamine was successfully treated with prenalterol, a new cardioselective beta-agonist. The case is discussed with respect to plasma concentrations of dopamine, prenalterol and amitriptyline. Prenalterol, hydrocortisone and insulin may be useful as inotropic agents in tricyclic poisoning where dopamine fails to provide an adequate response.

Adrenergic beta-Agonists↗
PubMed1981

Unusual 'spike-wave stupor' in a patient with manic-depressive psychosis treated with amitriptyline.

'Spike-wave stupor' was observed in a 58-year-old male patient with manic-depressive psychosis. Almost continuous atypical spike-wave activity was seen in conjunction with a stuporous episode with stereotyped automatism. Intravenous diazepam ended both the electroencephalographic epileptiform discharges and the clinical stupor. Before and during this episode the patient was treated with an average-dose amitriptyline monotherapy. There was no family history of epileptic seizures. The patient had had electroconvulsive therapy. The history suggests that the analeptic property of amitriptyline induced the 'spike-wave stupor' in this patient.

Action Potentials↗
PubMed1982

Effects of amitriptyline on serum glutamate and free tryptophan in rats.

In rats, chronic amitriptyline (14 days, 10 mg/kg, IP) administration resulted in a significant increase in the serum glutamate concentration and concomitant increase in the serum free tryptophan. In contrast, amitriptyline had no effect on the total serum tryptophan or CSF glutamate level. The data confirmed that antidepressant drugs may induce an increase of the serum glutamate concentration in depressive patients.

Amitriptyline↗
PubMed1977

Noradrenaline, depressive illness, and the action of amitriptyline.

The tyramine-dose/pressor response test was carried out on a series of patients suffering from primary depressive illness before and during treatment with amitriptyline. The severity of their depression was assessed during the study of the Hamilton Rating Scale (HRS). The decreased tyramine sensitivity induced by the drug, which is related to the inhibition of NA reuptake, correlated significantly with the plasma concentration of nortriptyline. However, contrary to the expectation of the noradrenaline hypothesis of depression, the decreased tyramine sensitivity, i.e., the degree of NA-reuptake blockade, did not show any correlation with clinical improvement following 6 weeks' treatment with amitriptyline.

Adult↗
PubMed1979

The effect of amitriptyline and mianserine (Org. GB94) on food motivated behaviour of rats trained in a runway: possible correlation with biogenic amine concentration in the limbic system.

Rats on a 23 h food deprivation schedule were trained to run down a straight runway for a food reward. Neither amitriptyline nor mianserine had an effect on the running time for the food reward during the period of continuous reinforcement. However both antidepressants delayed the extinction of this response. It seems unlikely that this effect on extinction was due to an altered motivation for the food reward as amitriptyline significantly decreased the food intake of the experimental animals while mianserine increased the food intake throughout the period of the experiment. The observation that both these antidepressants reduce the speed of extinction of rewarded behaviour may be explicable in terms of observed changes in the concentration of biogenic amines in the limbic system.

Amitriptyline↗
PubMed1978

Effects of chlordiazepoxide, amitriptyline, imipramine, and their combinations on avoidance behaviour in mice.

Chlordiazepoxide, imipramine, and amitriptyline, given alone or in combination, were tested in mice subjected to 5 daily 100-trial avoidance sessions in the shuttle-box. When the drugs were given alone, chlordiazepoxide and the lower doses of imipramine facilitated avoidance behaviour. The higher doses of the two antidepressants impaired avoidance behaviour. Mixtures of chlordiazepoxide and imipramine produced some facilitating effects, while depressant effects prevailed in the chlordiazepoxide-amitriptyline combinations.

Amitriptyline↗
PubMed1975

The effect of amitriptyline, desipramine and imipramine on the vivo brain synthesis of 3H-noradrenaline from 3H-L-dopa in the rat.

3H-L-Dopa was given to rats after a peripheral decarboxylase inhibitor Ro 4-4602 (50 mg/kg) and the effect of 30 min pretreatment with antiptyline (10 mg/kg), desipramine (10 mg/kg) and imipramine (10 mg/kg) on the brain formation of 3H-dopamine, 3H-noradrenaline and their major metabolites was investigated. Desipramine produced a decrease in the level of labelled noradrenaline and its major metabolites free and conjugated 3-methoxy-4-hydroxyphenyleneglycol and 3,4-dihydroxyphenyleneglycol. Imipramine decreased labelled noradrenaline and 3-methoxy-4-hydroxyphenyleneglycol, whereas amitriptyline produced no significant effect on noradrenaline metabolism. The thymoleptic drugs produced no significant effect on endogenous brain noradrenaline and dopamine. These findings provide a strong indication that desipramine and imipramine inhibit the 3H-noradrenaline biosynthesis from 3H-L-Dopamthe effect seems closely related to the well-known membrane inhibitory effect of these drugs, since desipramine produced a more marked effect than imipramine and amitriptyline showed no effect. No conclusive evidence for the precise mechanism of action was obtained but it is possible that the decreased 3H-noradrenaline synthesis is related to interference of desipramine and imipramine with the precursor (s) 3H-L-Dopa or 3H-dopamine at sites of 3H-noradrenaline biosynthesis.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Amoxapine and amitriptyline. I. Relative speed of antidepressant action.

Speed of onset of antidepressant effect was studied in 20 depressed outpatients assigned double-blind to equipotent doses of amoxapine or amitriptyline. In counter-balanced order, each patient had 2 periods of 3 weeks on active agent interspersed with 2 similar periods of placebo control. On daily and weekly self-ratings, amoxapine was found to reduce symptoms significantly more rapidly than amitriptyline. Psychiatrist-ratings were consonant with self-reports.

Adult↗
PubMed1985

Cianopramine and amitriptyline in the treatment of depressed patients--a placebo-controlled study.

3-Cyano-imipramine (cianopramine) is a potent and selective inhibitor of serotonin uptake into synaptosomes. In a double-blind trial, 60 patients with various types of depression fulfilling the DSM-III criteria of depressive episodes were treated with either cianopramine (n = 20, mean daily dose 3.3 +/- 0.6 mg) amitriptyline (n = 20, mean daily dose 86.4 +/- 21 mg) or placebo (n = 20) orally. According to the ratings of the Hamilton Scale of Depression and clinical global evaluations, both active drugs showed statistical superiority over placebo (P less than 0.02). The frequencies of anticholinergic side effects in the cianopramine group were comparable to those of the placebo group and were less than in the amitriptyline group. The findings suggest that cianopramine is a promising new antidepressant.

Adjustment Disorders↗
PubMed1985

Cardiovascular effects of amitriptyline in the treatment of elderly depressed patients.

Thirteen elderly depressed patients (age 60-82 years) were treated for 5 weeks with a fixed dose of amitriptyline 100 mg (sustained release preparation). In all patients the sum of concentrations of amitriptyline and nortriptyline exceeded 130 micrograms/l, which is the recommended plasma level. Cardiovascular side effects were recorded by monitoring heart rate, blood pressure, standard ECG and systolic time intervals. During treatment, a transient increase in the supine heart rate was observed without significant changes in the supine blood pressure. The orthostatic drop in blood pressure was markedly increased during treatment without a compensatory increase in heart rate, and these changes remained significant during the whole investigational period. PQ and QRS were significantly increased during treatment, and significant changes in the systolic time intervals were found indicating impairment of myocardial conduction and contractility. In three patients medication was discontinued due to cardiovascular side effects.

Aged↗
PubMed1982

Growth hormone release after acute amitriptyline administration to normal human subjects.

Single doses of the antidepressant amitriptyline were given to 12 normal males. After parenteral or oral dose of the drug, the concentration of growth hormone in plasma rose in one third of the subjects. Amitriptyline could have multiple and potentially opposite pharmacological actions on growth hormone. Antidepressants appear to be poor pharmacological tools for assessing the regulation of growth hormone release.

Administration, Oral↗