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PubMed1982

Cardiac sensitivity to the inhibitory effects of chlorpromazine, imipramine and amitriptyline upon formation of flavins.

Chlorpromazine, imipramine and amitriptyline, drugs structurally related to riboflavin, each inhibited the formation in vivo of flavin adenine dinucleotide (FAD) from riboflavin in rat heart at 2-5 mg/kg body weight, doses comparable on a weight basis to those used clinically. All three drugs inhibited FAD formation in heart within 5 hr after a single dose of 25 mg/kg. Chlorpromazine under these conditions also inhibited FAD formation in liver, cerebrum and cerebellum. A series of psychoactive agents structurally unrelated to riboflavin did not inhibit flavin formation in the organs tested. These findings indicate that the inhibitory effects of the drugs studied have organ specificity with respect to FAD formation.

Amitriptyline↗
PubMed1988

Chronic treatment with amitriptyline produces supersensitivity to nicotine.

The authors used a thermoregulation paradigm to evaluate effects of amitriptyline (AMI) on the sensitivity of a nicotinic mechanism involved in the regulation of core temperature in rats. Treatment with this tricyclic was associated with a significant increase in the hypothermic response to nicotine. Supersensitivity persisted for a minimum of 7.5 days following the last dose of AMI, and a significant proportion of animals displayed increased sensitivity after 14.5 days of abstinence. Implications for the mechanism of action of AMI are highlighted.

Amitriptyline↗
PubMed1993

Increase in number of LHRH neurones in septal-preoptic area of rats following chronic amitriptyline treatment: implication in antidepressant effect.

Recent studies have implicated the peptide LHRH in a variety of actions including a role in modulation of affective behavior. The present study has been undertaken to determine its involvement in the action of antidepressants, if any, using amitriptyline (AMT) as the model antidepressant drug. The repeated administration of AMT (10 mg/kg/day) in rats increased the number of LHRH neurones in the septal-preoptic area. While 1 week of AMT treatment slightly augmented the number of LHRH neurones, the rise was not statistically significant, however, following 2 weeks of AMT treatment, a significant (P < 0.05) increase (41.05%) was observed. Three and four weeks of AMT treatment further increased the number of neurones by 60.84% and 72.96% respectively; a remarkable rise in the LHRH immunoreactivity around organum vasculosum of lamina terminalis (OVLT) was also noticed. Acute AMT treatment had no effect on the number of neurons; however, the intensity of immunoreaction in the OVLT was slightly decreased. In the behavior despair test, a single dose of AMT displayed an immobility reducing effect which was also shown by a single dose of LHRH (1 mg/kg). The combination of LHRH (1 mg/kg) and AMT also reduced the immobility; the effect was the same as one produced by each drug given separately. The results suggest that chronic AMT treatment may induce transcription and translation in LHRH cells and that the peptide LHRH may be involved in the mediation of the antidepressant effect, characteristic of AMT.

Amitriptyline↗
PubMed1981

Simultaneous liquid chromatographic analysis of amitriptyline, nortriptyline, imipramine, desipramine, doxepin, and nordoxepin.

A simultaneous method for the therapeutic monitoring of amitriptyline, doxepin, imipramine, and their active demethylated metabolites nortriptyline, nordoxepin, and desipramine, respectively, in plasma or serum by reversed-phase liquid chromatography (RPLC) is presented. The drugs and the internal standard (loxapine) are first extracted from 2 ml of serum into butylchloride at pH 14, and then back extracted into 200 microliter of 0.025 mol/l hydrochloric acid. An aliquot of the aqueous acid phase is injected into the chromatograph and eluted with acetonitrile-phosphate buffer (21: 79, by vol.) containing 0.6 nl of n-nonylamine per liter of phosphate buffer. The drugs are eluted in a total chromatographic time of approximately 13 min at ambient temperature and detected at 200 nm. A sensitivity of 5 microgram/l of serum for each drug is obtained. Recoveries for these drugs ranged from 77% to 103%; and the coefficient of variation (day-to-day) ranged from 4.2 to 7.8. Of 35 basic or neutral drugs tested for possible interference, only propoxyphene interferes with the analysis of nortriptyline.

Amitriptyline↗
PubMed1986

Enzyme-linked immunosorbent assay for amitriptyline and other antidepressants using a monoclonal antibody.

We describe and evaluate a method to measure amitriptyline and other tricyclic antidepressants by enzyme linked immunosorbent assay, using monoclonal antibody. In this assay, biological samples were first incubated with the antibody; in a second step, free remaining antibody was allowed to bind to lysozyme-nortriptyline coated immunotitration plates. The bound fraction of the monoclonal antibody was revealed with rabbit anti-mouse serum coupled to horseradish peroxidase. The optical density of the reaction product was measured with a colorimeter at 410 nm. Specificity of the antibody was investigated by means of a Farr test showing interferences in therapeutic ranges only for chlorpromazine and phenytoine. Means of intra- and inter-assay variations were 10 and 13%, respectively. The results when compared to those obtained by gas chromatography with a selective nitrogen detector gave a correlation coefficient of 0.897. Finally, the great reliability of the monoclonal antibody, the advantages of a decreased analysis time, low cost and high capacity of the procedure contribute to make this immunoassay most suitable for clinical monitoring and pharmacokinetic studies of tricyclic antidepressants.

Amitriptyline↗
PubMed1987

Therapeutic drug monitoring of amitriptyline: impact of age, smoking and contraceptives on drug and metabolite levels in bulimic women.

Concentrations of amitriptyline (AT), nortriptyline (NT) and E-10-hydroxynortriptyline (E-10-OH-NT) were measured in 18 women with bulimia receiving 100 mg AT/day for at least 6 wk. After onset of treatment between days 36 and 57 there is a decrease in AT and an increase in E-10-OH-NT concentrations, probably due to an autoinductive effect on hydroxylation. The estimated mean (+/- SD; range; n) elimination half-life time of AT was 14.0 (+/- 7.8 h; 7.5-38.5 h; 14). On day 36, AT concentrations in females using oral contraceptives (OC) were higher than in non-users of OC, which indicates inhibition of AT metabolism by OC. In all smokers the E-10-OH-NT concentrations on day 36 were lower than in non-smokers. Our findings suggest induction of N-demethylation and glucuronidation by smoke components.

Adolescent↗
PubMed1987

Changes in urinary catecholamines and their metabolites in depressed patients treated with amitriptyline or imipramine.

The effects of treatment with amitriptyline (AMI) or imipramine (IMI) on changes in catecholamines and their metabolites in urine were studied in 95 unipolar and bipolar depressed patients. For the entire group, not separated by drug, substantial reduction in concentrations of all metabolites, but not catecholamines, occurred. Although catecholamine and metabolite change was similar for most substances assayed, there were some specific drug and diagnostic group differences. Vanillylmandelic acid (VMA) reduction was limited to bipolar patients; metanephrine (M) reduction to unipolar patients. Greater M and 3-methoxy-4-hydroxyphenylglycol (MHPG) reduction were associated with response in unipolar, but not bipolar patients. In bipolar, but not unipolar patients, norepinephrine (NE) rose in responders in contrast to reductions among nonresponding bipolar patients. The results suggest that effectiveness of blockade of reuptake of norepinephrine may be relatively more important for recovery in bipolar than in unipolar patients. Study of a battery of amine substances may contribute more information to our understanding of antidepressant drug effects on aminergic systems than analyses of MHPG alone.

Adult↗
PubMed1993

Effect of amitriptyline on neurotransmitter levels in adult mice following infection with the avirulent strain of Semliki Forest virus.

Infection of adult mice with the avirulent strain of Semliki Forest virus (SFV) led to neurochemical abnormalities, notably depressed levels of catecholamines (CATs) such as noradrenaline (NA), adrenaline (A) and 3-methoxy-4-hydroxyphenylglycol (MHPG) (a metabolite of NA) particularly in the hypothalamus and the inferior colliculus but not in the temporal cortex. In addition, depressed levels of NA and A were also found in the cerebrospinal fluid (CSF) and the serum. Administration of a tricyclic antidepressant drug, amitriptyline, kept the levels of NA, A and MHPG similar to those of the saline-treated control mice in the hypothalamus, inferior colliculus and CSF.

Amitriptyline↗
PubMed1983

Chronic amitriptyline potentiates feeding induced by intrahypothalamic norepinephrine injections.

Feeding responses to microinjections of 37 nmol norepinephrine (NE) into the medial hypothalamus of rats were assessed before and after chronic amitriptyline treatment (AMI, 10 mg/kg twice daily for 21 days). AMI-treated rats showed a 55% increase in NE-induced feeding over their pre-treatment baseline. Control rats which received daily vehicle injections showed only a non-significant 3% increase on retests. These results are consistent with recent evidence suggesting that chronic AMI may enhance the responsivity of postsynaptic alpha adrenoceptors. The data also suggest that altered hypothalamic NE mechanisms may contribute to the enhanced appetite changes reported by patients undergoing long-term AMI treatment.

Amitriptyline↗
PubMed1994

Site- and test-dependent antinociceptive efficacy of amitriptyline in rats.

The antinociceptive efficacy of systemic- (IV), spinal- (IT), and global supraspinal (ICV)-administered amitriptyline (AMIT) was compared in three different tests for nociception: the hot-plate test, the tail-flick test, and the withdrawal reflex test. Systemic AMIT inhibited the responses in each of the three tests, with distinct dose-effect relationships. Spinal AMIT reduced in a dose-dependent fashion the force of withdrawal to noxious electrical stimulation but was ineffective in the hot-plate test and facilitated the responses in the tail-flick test. Supraspinal AMIT inhibited in dose-dependent fashion the response to the stimulus of the hot plate, reduced the force of withdrawal after a dose that was effective by the IV route, and again facilitated the responses in the tail-flick test. The results suggest that spinal sites mediate the inhibition of the withdrawal reflex and the supraspinal site the inhibition of the hot-plate test. Two conclusion are drawn: First, AMIT's site of action varies among the pain modalities; and, second, augmentation of the reactions can occur. The complex interaction accords with the clinical experience that the benefits of AMIT in pain treatment are hard to predict.

Amitriptyline↗
PubMedDate not supplied

Leu-enkephalin content in rat brain during prolonged treatment with imipramine or amitriptyline.

Male Wistar rats were treated with imipramine /IMI/ /2 or 10 mg/kg, p.o./ or amitriptyline /AMI/ 10 mg/kg, p.o./ by drinking water. Each drug was given once or over periods of 1, 3, 4, 6 and 9 months. Leu-enkephalin /LENK/ content was measured by radioimmunoassay in the striatum, hypothalamus and brain perfusates after different periods of the treatment with antidepressants. A single 10 mg/kg dose of IMI increased the level of LENK in the striatum and decreased it in the hypothalamus. Six months after IMI treatment the level of LENK in the striatum was decreased after a 2 mg/kg dose and increased after 10 mg/kg; in the hypothalamus a dose-dependent increase of LENK content was observed. In brain perfusates the level of LENK was decreased 3 months after IMI treatment, but highly increased after a 9-month administration. This indicates that during prolonged treatment with imipramine the central enkephalinergic activity is dynamically changed and can affect the psychopharmacological effects of IMI. After the prolonged treatment with AMI a decrease of LENK level in the striatum was observed only after 4 months of the drug administration, and no changes were seen in the hypothalamus. It is suggested that both antidepressants studied have different action on the central enkephalinergic system.

Administration, Oral↗
PubMed1980

Symptoms as predictors of response to amitriptyline and nortriptyline -- the plasma level variable.

Data collected to define therapeutic plasma levels for amitriptyline and nortriptyline were re-analyzed to test endogenous and non-endogenous symptoms as response predictors while controlling for plasma level variable. The selection criteria limited the range of historical predictors. Initial symptom quality was not predictive of outcome for the entire group of 44 patients or for the 27 with therapeutic plasma levels. Delusions were not associated with poor outcome. The authors conclude that historical components of the endogenous--non-endogenous distinction (e.g., premorbid personality, stability of symptoms over time, quality of remissions) may be more important as response predictors.

Amitriptyline↗
PubMed1985

Cerebrospinal fluid levels of amitriptyline, nortriptyline, imipramine and desmethylimipramine. Relationship to plasma levels and treatment outcome.

Fifty-five (55) depressed patients were treated with amitriptyline (AMI) or imipramine (IMI). Concentrations of AMI, IMI, and their metabolites, nortriptyline (NT) and desmethylimipramine (DMI), were measured in cerebrospinal fluid (CSF) and plasma at steady state by gas chromatography mass spectrometry (GC/MS). Highly significant correlations between CSF and plasma levels of AMI, NT, IMI, and DMI were found (r greater than 0.75; P less than 0.0001 in all cases). There were no significant sex, diagnostic subgroup, or geographic difference in any of the drug parameters measured. An evaluation of the relationship between CSF levels of drug variables and clinical response showed essentially no significant correlations between these various parameters. The results obtained do not support the concept of a 'therapeutic window' for levels of plasma NT in AMI-treated patients. Furthermore, the highly significant correlations between CSF and plasma compartments in terms of drug and metabolite levels would argue against the need to measure CSF levels of these parameters in clinical practice. Plasma level measurements should be equally informative, and simpler to obtain.

Amitriptyline↗
PubMedDate not supplied

Hypochondriacal fears and beliefs in DSM-III melancholia. Changes with amitriptyline.

The authors administered the Illness Attitude Scales, which identify hypochondriacal patients, to 20 nonpsychotic inpatients with DSM-III diagnosis of melancholia before and after 4 weeks of treatment with amitriptyline, and to a matched group of normals. Before treatment characteristic hypochondriacal responses occurred in over one-third of melancholics whereas after treatment the number was the same as in normals. The findings are in accord with the clinical observation that melancholia is one of the causes of hypochondriacal fears and beliefs and these tend to remit with recovery from depression.

Adult↗
PubMedDate not supplied

Ethological predictors of amitriptyline response in depressed outpatients.

Non-verbal behaviour of 22 unipolar, non-delusional depressed outpatients was video-recorded during psychiatric interview to determine whether response to tricyclic treatment (50-100 mg/day of amitriptyline for 5 consecutive weeks) could be predicted on the basis of the ethological profile at baseline. At the end of the study, patients were divided into two treatment outcome groups on the basis of their final Hamilton Depression Rating Scale (HDRS) scores. At baseline, responders (n = 14, HDRS score less than or equal to 10) and non-responders (n = 8, HDRS score greater than 10) did not differ with respect to sex, age, education, DSM-III diagnosis, and HDRS score. In contrast, ethological profiles of the two treatment outcome groups at baseline were different, with non-responders showing significantly more assertive and affiliative behaviours. The results are discussed in the light of previous studies which have identified subgroups of depressive patients with different responsiveness to tricyclic treatment.

Adult↗
PubMed1993

Fluoxetine, amitriptyline and the electroencephalogram.

Electroencephalograms recorded before and after 4 weeks treatment of depressed patients with fluoxetine or amitriptyline were assessed visually and by power spectrum analysis blind to patient, treatment and whether the recordings were carried out before or after treatment. No significant between-group differences in alpha, beta or theta activity were found on visual assessment. Power spectrum analysis revealed a significant decrease in the amount of beta activity at week 4. There was no EEG evidence of drowsiness or epileptiform activity in either of the treatment groups.

Adult↗
PubMed1994

The pattern of physical symptom changes in major depressive disorder following treatment with amitriptyline or imipramine.

The study describes a sequential analysis of depression-related physical symptoms and their relationship to imipramine and amitriptyline plasma levels over 4 weeks of treatment in 79 unipolar and bipolar patients hospitalized for major depressive disorder. Insomnia diminished in all patients after 2 weeks of drug administration. After 4 weeks, the sleep of patients whose depressive disorder has significantly improved was nearly normal, whereas patients who remained depressed showed continued sleep impairment. Reductions in loss of appetite, weight and sexual interest paralleled mood improvement. Tricyclic plasma levels significantly correlated with improved sleep. The findings suggest a close link between depressed mood and physical symptoms during recovery from major depressive disorder.

Adult↗