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PubMed1977

[The "stimulatory proteodyschylia" in the amitriptylin (Laroxyl) treated rat parotid gland. Experiments on the effect of antidepressive pharmacotherapy on the parotid glands of the rat (author's transl)].

The activity of total amylase and isoamylases in the rat parotid gland is reduced by treatment with Amitriptylin (Laroxyl) for 3 and 7 days while the protein content of the glands remains constant. These changes are no longer visible after treatment for 21 days and following a period without drug application. To differentiate the disturbances of protein secretion (proteodyschylia) prominent in the clinical picture of sialadenosis, the following classification is proposed. We suggest the term "stimulatory proteodyschylia" for a decrease of acinar amylolytic activity, here caused by Amitriptylin application, as opposed to the "inhibitory proteodyschylia" characterized by an acinar amylase congestion.

Amitriptyline↗
PubMed1978

The effect of acute and chronic desipramine and amitriptyline treatment on rat brain total 3methoxy-4-hydroxyphenylglycol.

The effect of acute (single dose), short-term (4 days), and chronic treatment (21 days) with two tricyclic antidepressants desipramine and amitriptyline on brain 3-methoxy-4-hydroxyphenylglycol (MHPG) was examined in the rat. Amitriptyline had no effect on brain total MHPG irrespective of the duration of the treatment and did not interfere with the lowering effect of clonidine on brain total MHPG. Acute and short-term desipramine treatment decreased brain total MHPG in rats, while chronic desipramine treatment increased it. The differential effect of acute and chronic treatment of desipramine on the brain total MHPG was further demonstrated by the lack of interference with the lowering effect of clonidine on brain total MHPG by one single dose of desipramine; partial interference after 4 days and complete interference after 21 days of desipramine treatment.

Amitriptyline↗
PubMed1981

Comparison of the antimuscarinic activity of mianserin and amitriptyline in the cat superior cervical ganglion.

The antimuscarinic activity of mianserin and amitriptyline was investigated in the cat superior cervical ganglion using McN-A-343 as a muscarinic agonist. Mianserin was found to have a similar order of potency to amitriptyline in this preparation, in contrast to the marked difference in their antimuscarinic activities on non-neuronal muscarinic receptors. These findings suggest that the action of mianserin on neuronal muscarinic receptors is more important than that predicted from studies on non-neuronal receptors and may be related to its anti-depressant activity.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1983

Clinical investigations into antidepressive mechanisms. I. Antihistaminic and cholinolytic effects: amitriptyline versus promethazine.

It is assumed that established antidepressants exert their clinical efficacy by potentiation or decrease of central noradrenergic and serotonergic neurotransmission. However, recent experimental work suggests that antihistaminic and/or cholinolytic effects may also be involved. This double-blind controlled study compared amitriptyline (catecholamine potentiating, antihistaminic, cholinolytic) with promethazine (antihistaminic, cholinolytic) in 50 severely depressed inpatients over a 30-day treatment period. Analysis of the Hamilton depression rating scale revealed significant clinical superiority of amitriptyline over promethazine in such major depressive symptoms as depressed mood, suicidal ideation, psychic anxiety, and sleep disturbances. No significant difference was evident as far as autonomous side effects were concerned. Similar results were found by analysis of the AMP rating system. It is concluded that antihistaminic or cholinolytic effects per se do not explain the antidepressants' efficacy. However, potentiation of noradrenergic neurotransmission by cholinolytic activity might be the major antidepressive mechanism.

Adult↗
PubMed1980

Decreased tyramine sensitivity after discontinuation of amitriptyline therapy. An index of pharmacodynamic half-life.

A combined pharmacodynamic and pharmacokinetic approach was made to study the pharmacodynamic half-life (Pd1/2) of amitriptyline (AT). Six depressed patients were treated with 150 mg of amitriptyline as a single oral dose at night for six or more weeks. Decreased tyramine sensitivity (DTS), an index of this drug's pharmacological activity, was determined serially at various intervals after the last dose. Plasma concentrations of AT and nortriptyline (NT) were also estimated at above intervals. It was possible to detect DTS for 228-300 h after the last oral dose and the mean Pd1/2 of this decline of pharmacodynamic effect was observed to be 135 h. However, no measurable amount of AT or NT was present after 84 h and the mean elimination plasma half-life (t1/2) of AT and NT were 37.7 and 38.9 h, respectively. (In this study, pharmacokinetic parameters of NT were directly related with those of AT.) Prolonged pharmacodynamic effect of this drug after discontinuation should be borne in mind in order to avoid drug interactions and autonomic complications, especially after overdosage. Pd1/2, as assessed by DTS, correlated directly with the t1/2 (r = 0.91) and inversely with the plasma clearance rate (r = 0.60) of NT. DTS test can be used as an alternative technique to assess the biological activity of a drug which inhibits noradrenaline reuptake mechanism and/or blocks alpha-adrenoceptors at the peripheral neuronal sites, especially, where facilities to measure plasma concentrations of such drugs are limited.

Adult↗
PubMed1977

Cerebrospinal fluid amine metabolites after combined amitriptyline-triiodothyronine treatment of depressed women.

Levels of 5-hydroxyindoleacetic acid and homovanillic acid were measured in cerebrospinal fluid from 33 depressed women with no clinical response to amitriptyline, before and after combination treatment with triiodothyronine. Although the latter showed significant clinical improvement, changes in CSF amine metabolites did not differ significantly from a control group of 16 therapy-resistant depressed women receiving higher doses of amitriptyline. Possible explanations for the mechanism of action of triiodothyronine are discussed.

Adult↗
PubMed1991

Effects of chronic lithium, amitriptyline, and electroconvulsive shock, on calcium channel binding in a rat brain homogenate.

The effect of chronic lithium (0.1% in the diet for 28 days), amitriptyline (10 mg/kg SC daily for 14 days), and electroconvulsive shock (ECS) (given 5 x under halothane anaesthesia on alternate days) on the binding of the L-type calcium channel antagonist (+)-(3H)-PN 200-110 to rat cortical and hippocampal homogenates and the binding of the N-type calcium channel antagonist (125I)-omega-conotoxin to rat cortical homogenates was measured. These treatments did not alter the number or affinity of the binding sites for either ligand, suggesting that it is unlikely that the actions of chronic lithium, amitriptyline, and ECS affect calcium channel binding.

Amitriptyline↗
PubMed1987

Antidepressants for cancer pain and other painful syndromes with deafferentation component: comparison of amitriptyline and trazodone.

The Authors report a clinical multicentre experience with antidepressant agents (trazodone and amitriptyline) in the treatment of chronic cancer pain with deafferentation component. Forty-five patients were admitted to the study: 27 with oncological peripheral nerve lesions, 6 with post herpetic neuralgias, 10 with not oncological nerve lesions, 2 with central nervous lesions. Almost all of them were already being treated with NSAID associated 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, weakness were all taken into consideration. The therapeutic analgesic efficacy of the two drugs proved to be similar.

Adult↗
PubMedDate not supplied

Plasma and brain pharmacokinetics of amitriptyline and its demethylated and hydroxylated metabolites after acute intraperitoneal injection in mice.

The fate of amitriptyline (AMI) and its demethylated and hydroxylated metabolites was studied in Swiss CD1 mice, after acute intraperitoneal injection of AMI (20 mg/kg). Levels of each compound were determined to establish pharmacokinetic parameters in plasma and brain. Absorption and elimination of AMI were rapid (tmax = 0.37 h and 0.42 h, and t1/2 = 3.2 h and 3.6 h in plasma and brain, respectively). In plasma, 10-OH-nortriptyline was the main metabolite (46% of AUC) and 10-OH-amitriptyline reached significant levels but only during the first hour. In brain, AMI (43% of total AUC), nortriptyline (NOR) (29%) and demethylnortriptyline (DM-NOR) (11%) were the most abundant compounds, possibly through high blood-brain barrier transfer and/or marked intracerebral demethylation. Brain OH-metabolite levels were much lower. Knowledge of kinetic parameters and metabolism of AMI can help in the evaluation of pharmacological activity.

Amitriptyline↗
PubMed1998

[Unmasking pheochromocytoma by amitriptyline].

A report is given about a 57-year-old woman with a major depression, melancholic subtype. While under amitriptyline 75 mg/day no adverse effects were observed, immediately after increasing the dosage to 150 mg/day "head spasms" with headache, profuse sweating and arterial hypertension appeared. The diagnosis of a pheochromcytoma was made and adrenalectomy was performed. This is the first case of unmasking a pheochromcytoma by amitriptyline; furthermore a connexion was found with the daily dosage of the antidepressant.

Adrenal Gland Neoplasms↗
PubMed2001

[Non-fatal effect of highly toxic amitriptyline level after suicide attempt. A case report].

Pharmacotherapeutic intervention in psychiatric patients often bears the risk of drug abuse for suicide attempts. Especially intoxication with tricyclic antidepressants, e.g., amitriptyline, may cause severe complications such as cardiac arrhythmia. Even under intensive care conditions, 2-3% of intoxicated patients still die. Here, we report on a depressed female patient who, thanks to timely and intense intervention, survived a suicide attempt with amitriptyline despite highly toxic plasma levels.

Adult↗
PubMed1986

Amitriptyline normalizes tetrabenazine-induced changes in cerebral microcirculation.

The cerebromicrocirculation in the tetrabenzaine (TBZ) model of depression has been found to be abnormal with respect to (1) responsiveness of cerebral blood flow to increases in arterial CO2 content and (2) the effective permeability of the blood-brain barrier to water. Development of these abnormalities temporally paralleled the behavioral disturbances and catecholamine depletion induced by TBZ. These TBZ-induced changes occurred globally throughout the brain, being apparent in the forebrain, cerebellum, and medulla-pons. Pretreatment with the antidepressant amitriptyline prevented both behavioral and physiological effects of TBZ, whereas amitriptyline administered after TBZ was less effective. The results suggest that an important action of tricyclic antidepressants may be cerebromicrocirculatory effects.

Amitriptyline↗
PubMed1991

Longitudinal effect of amitriptyline and fluoxetine treatment on plasma phenylacetic acid concentrations in depression.

Unconjugated (U-PAA), conjugated (C-PAA), and total phenylacetic acid (T-PAA) concentrations in blood plasma and monoamine oxidase (MAO) activity in platelets towards phenylethylamine (PE) were determined in 40 drug-free, depressed patients (23 melancholic, 17 nonmelancholic) from five psychiatric treatment centers, and in 34 normal healthy volunteers. No significant differences were found between controls and all depressed patients or between melancholic and nonmelancholic depressed patients. Treatment of the depressed patients with amitriptyline or fluoxetine over a 6-week period resulted in clinical improvement and in a significant increase in plasma PAA concentrations. A decline in the Beck and Hamilton rating scores during treatment correlated significantly with increases in the concentrations of unconjugated, conjugated, and total phenylacetic acid but not with MAO activity, which did not change during treatment. At each of the three assessment times, however, plasma PAA concentrations and psychiatric rating scores were not significantly correlated. Except for higher end-of-study T-PAA concentrations in the amitriptyline-treated subjects, no significant differences were found between the effects of the two drugs with regard to plasma phenylacetic acid levels, MAO activity, or rating scores.

Adult↗
PubMed1992

Biochemical measures in patients with a somatoform pain disorder, before, during, and after treatment with amitriptyline with or without flupentixol.

The possible relationship between a number of biochemical parameters and measures of pain and depression was studied in chronic pain patients without a major depression. In a double-blind crossover study, patients were treated with amitriptyline combined with a low dose of flupentixol or placebo. We investigated whether pretreatment biochemical values correlated with initial data on pain and/or depression, or whether they had predictive value for treatment outcome. We also studied systematically the effect of both treatment regimes on the biochemical parameters themselves and their relation to the plasma levels of amitriptyline. From our results, the possible involvement of the serotonin system in somatoform pain disorder is confirmed and no direct relation with the noradrenergic system could be inferred. The lack of involvement of a number of putative, depression-related, biochemical parameters suggests that affective disorders and pain syndromes do not share all mechanisms in common.

Adult↗
PubMed1988

The effect of amitriptyline on growth of olfactory and cerebral neurons in vitro.

The tricyclic antidepressant drug amitriptyline has a detrimental effect on neurite outgrowth in primary explant cultures containing either olfactory receptor neurons or cerebral neurons, from both rat and chick embryos. When the drug is added to the culture medium in doses similar to the plasma concentrations known to be therapeutic in humans, the number of explant cultures expressing neurites is significantly reduced. In higher doses, amitriptyline reduces the amount of olfactory marker protein synthesized by organ cultures of olfactory mucosa.

Amitriptyline↗
PubMed1984

The effect of zimelidine and amitriptyline on the brain concentration of some indolic and phenolic monoamines in the mouse.

The increase in mouse brain tryptamine accumulation rate and 5-hydroxytryptamine (5-HT) concentration and the reduction in 5-hydroxyindole acetic acid concentration observed after zimelidine administration suggest that the treatment reduces the brain tryptophan availability. Amitriptyline produced no significant changes on tryptamine, 5-HT or 5-hydroxyindole acetic acid. Also, zimelidine reduced mouse brain p-tyramine, increased m-tyramine and increased homovanillic acid. Similar effects were observed after amitriptyline administration. The experiments show that both drugs affect dopamine turnover and tyramine concentration in a similar fashion to that observed for the antipsychotic group of drugs, thus suggesting that they may have some antipsychotic effects, especially if administered at the high dose levels. In addition, it may also possess some of the undesirable effects of this group of drugs.

Amitriptyline↗
PubMed1989

In vivo action of phosphatidylserine, amitriptyline and stress on the binding of [3H]imipramine to membranes of the rat cerebral cortex.

Liposomes of bovine brain phosphatidylserine and of phosphatidylcholine were prepared and injected i.p. into rats for 5 days. Another group received i.p. injections of amitriptyline in addition to phosphatidylserine. Subgroups of control and phosphatidylserine-injected rats were submitted to an acute swimming stress for 15 min. The number of [3H]imipramine binding sites in the phosphatidylserine-injected rats, decreased 23% whereas there was no change in the phosphatidylcholine-injected rats. The combination of amitriptyline and phosphatidylserine produced a more marked reduction in [3H]imipramine binding (-47%). Control rats undergoing acute stress showed a 30% decrease in [3H]imipramine binding whereas the stress did not significantly change the control values of the phosphatidylserine-treated animals. These findings are discussed in relation to the known action of phosphatidylserine on several neurotransmitter systems and on the potentiation of antidepressant effects.

Amitriptyline↗
PubMed1992

Amitriptyline produces analgesia in the formalin pain test.

A dose of 20 mg/kg of amitriptyline reduced pain in the second phase of the formalin test, which is an animal model of long-lasting pain in humans. Since the analgesic effect was produced by a single dose, which is insufficient to produce an antidepressant effect, these results indicate that amitriptyline has analgesic properties that are independent of its antidepressant properties.

Amitriptyline↗