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PubMed2000

Effects of trazodone on neurotransmitter release from rat mossy fibre cerebellar synaptosomes.

The effects of trazodone and putative sigma (sigma) receptor ligands were investigated on KCl-stimulated release of glutamate (Glu) and gamma-aminobutyric acid (GABA) from cerebellar mossy fibre synaptosomes. Both trazodone and serotonin (5-HT) inhibited the increase of Glu and GABA release evoked by 15 mM KCl. Trazodone increased the inhibition of Glu release caused by 0.01 microM 5-HT, while it antagonized the inhibition induced by higher 5-HT concentrations. Despite the low affinity of trazodone for both sigma(1) and sigma(2) binding sites, with a pK(i) of 5.9 and 6.0 respectively, two sigma receptor ligands, (+)-3-[3-hydroxypheny]-N-(1-propyl)piperidine ((+)-3-PPP) and N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine (BD 1047) antagonized the effects of trazodone. The putative sigma receptor ligand N-allylnormetazocine ((+)-SKF 10,047) mimicked the inhibitory effect of trazodone. As with trazodone, (+)-3-PPP and BD 1047 antagonized the activity of (+)-SKF 10,047 but not that of 5-HT. On the whole, these results suggest that trazodone shares a common molecular target with sigma compounds distinct from that of 5-HT and is involved in K(+)-stimulated Glu and GABA release from mossy fibre cerebellar synaptosomes.

Animals↗
PubMed2001

Effects of genetic polymorphism of CYP1A2 inducibility on the steady-state plasma concentrations of trazodone and its active metabolite m-chlorophenylpiperazine in depressed Japanese patients.

The effects of a genetic polymorphism of inducibility of cytochrome P450 (CYP) 1A2 on the steady-state plasma concentrations of trazodone and its active metabolite, m-chlorophenylpiperazine, were studied in order to clarify if these steady-state plasma concentrations are dependent on the CYP1A2 polymorphism. Fifty-eight Japanese depressed patients received trazodone 150 mg/day at bedtime. The steady-state plasma concentrations of trazodone and m-chlorophenylpiperazine were measured in duplicate using high performance liquid chromatographic method, and were corrected to the mean body weight for analyses. A point mutation from guanine (wild type) to adenine (mutated type) at position -2964 in the 5'-flanking region of CYP1A2 gene was identified by polymerase chain reaction fragment length polymorphism method. The mean steady-state plasma concentration of trazodone, but not m-chlorophenylpiperazine was significantly (P<0.05) lower in smokers than in non-smokers. Twenty-two smokers had 16 homozygotes of the wild type allele, 5 heterozygotes of the wild type and mutated alleles, and one homozygote of the mutated allele. There was no significant difference in the mean steady-state plasma concentration of trazodone or m-chlorophenylpiperazine between smokers with no mutation and those with mutation, although one homozygote of the mutated allele had the highest steady-state plasma concentration of trazodone in smokers. The present study thus suggests that CYP1A2 polymorphism does not necessarily have predictive value of the steady-state plasma concentration of trazodone or m-chlorophenylpiperazine in most of the smokers treated with trazodone.

Adult↗
PubMedDate not supplied

Investigation of a fatality due to trazodone poisoning: case report and literature review.

Trazodone is an antidepressant agent used in Spain since 1975. There are few documented reports of fatalities solely attributed to trazodone and none in which the main metabolite is analyzed. A fatal case of self-poisoning following oral ingestion is reported along with a description of the validated analytical methods involved, a discussion of poisoning characteristics, and a review of reports describing trazodone overdose cases with analytical results. The deceased was an 86-year-old man with cancer, who suffered depression. He went to see his doctor in a primary health care unit and told him he had just taken an unknown amount of tablets of Deprax to commit suicide. The doctor induced emesis as a first emergency measure. His death occurred before arriving to the hospital, and he left a suicide note nearby. Systematic toxicological analysis of postmortem blood used routinely in our laboratory revealed the presence of trazodone 4.9 mg/L and m-chlorophenyl-piperazine (m-CPP) 0.6 mg/L, its active and major metabolite. In addition, metamizol 19.6 mg/L and 4-methyl-amino-antipyrine (4-MAA) 40.7 mg/L, its active metabolite, were also found in blood. All drugs and metabolites involved in the case were detected using gas chromatography-nitrogen-phosphorus detection (GC-NPD) and confirmed using gas chromatography-mass spectrometry (GC-MS) mode total ion chromatogram. An additional high-performance liquid chromatography-diode array detection (HPLC-DAD) screening also obtained the same results. Quantitation of trazodone together with its metabolite in blood was carried out using GC-NPD, while quantitation of metamizol was performed using HPLC-DAD. Limits of detection for trazodone and m-CPP were 33 and 11 microg/L, respectively, absolute recoveries were more than 86% and 75%, respectively, intra-assay precisions less than 4%, interassay precisions less than 5%, and linearity up to 2.0 mg/L. Limit of detection for metamizol was 1117 microg/L, absolute recovery more than 84%, intra-assay precision less than 8%, interassay precision less than 12%, and linearity up to 48 mg/L. Based on the autopsy findings, patient history, toxicology results, and previously reported trazodone intoxications, the forensic pathologists ruled that the cause of death was due to an overdose of trazodone, and the manner of death was listed as suicide.

Aged↗
PubMed1989

Experimental examination of trazodone.

To establish the differential indication of trazodone and to find the predictors of its efficacy, we conducted a study in which 45 patients with major depressive disorder and 75 patients with acute schizophrenia were randomly assigned under double-blind conditions to either 400 mg trazodone daily, 150 mg amitriptyline daily, 20 mg haloperidol daily, or placebo daily. At the beginning of the investigations, numerous variables (basic data, MMPI, AMDP, HAM-A, HAM-D) were documented and evaluated on days 3, 7, 14, and 21. In our study, trazodone proved to be as effective an antidepressant drug as amitriptyline. In group comparison, no antipsychotic action of trazodone in schizophrenic patients could be proved. Yet the trazodone treatment was clearly of less risk than the amitriptyline treatment. Under trazodone, provocation of schizophrenic symptoms, which occurred numerously under amitriptyline, was found only in one patient out of 17 schizophrenics. Related to anamnesis and characteristics of the schizophrenic patient, a predictor-variable concerning the antipsychotic effect was not found. It can be assured, however, that patients with depressive symptoms (regarding the entity classification) respond to trazodone. After only 7 days of trazodone treatment, a relatively reliable decision can be established as to whether a therapeutical success can be expected if treatment is continued.

Adult↗
PubMed1984

The role of trazodone in the treatment of depressed cardiac patients.

The novel antidepressant trazodone is hypothesized to be less cardiotoxic than the tri-tetracyclic antidepressants. Recently, however, 2 patients with preexisting ventricular irritability showed an increased number of ventricular premature beats and of repetitive forms after starting on trazodone. Data are presented here from four studies on the cardiovascular safety of trazodone. Conclusions are: (1) Trazodone has little effect on cardiac conduction. (2) Trazodone does not worsen supraventricular arrhythmias. (3) Trazodone produces less postural hypotension than most other antidepressants and it tends to lower heart rate. (4) Lower doses of trazodone (100-300 mg) are better tolerated and more effective in major depressives simultaneously debilitated by significant cardiovascular disease. (5) It is possible that the so-called 'trazodone aggravation' of ventricular irritability is a statistical artifact--although further research is needed to verify this conclusion, and in the meantime the drug should be used with caution in such patients.

Aged↗
PubMed2001

Hepatotoxicity after short-term trazodone therapy.

OBJECTIVE: To report a case of severe hepatotoxicity from a four-day course of trazodone in a patient being treated according to protocol in a detoxification center. CASE SUMMARY: A 46-year-old HIV-positive man with a past medical history of intravenous drug abuse and hepatitis C, who was well controlled with HIV medications, was admitted for cocaine withdrawal. The patient was started on a standard protocol at the detoxification center with methadone 50 mg/d, clonidine 0.1 mg twice daily for four days, and trazodone 200 mg/d for four days. Laboratory results showed acute hepatitis and cholestasis five days following admission. Trazodone and clonidine were discontinued at that time. His methadone and HIV regimens remained unchanged. Liver function test results were greatly improved 10 days after trazodone and clonidine discontinuation. DISCUSSION: This is the first case report of trazodone-induced liver damage after only a few days of therapy. Previous reports describe hepatitis developing after weeks to months of trazodone therapy. All comorbidities thought to affect the described laboratory abnormalities were ruled out as a cause by a hepatologist. The observation of the sudden rise and fall of liver enzymes is characteristic of a drug reaction in the absence of trauma and severe shock. CONCLUSIONS: Due to the temporal relationship of the introduction and withdrawal of trazodone in the medication regimen and the elevations in liver enzymes, we conclude that this patient experienced acute hepatitis induced by trazodone 200 mg/d therapy for four days. The findings of this case warrant caution and closer monitoring in a patient with multiple risk factors for liver damage.

Adult↗
PubMed2005

[Trazodone and venlafaxine in treatment of depressive disorders].

UNLABELLED: In depressive disorders treatment a variety of antidepressant drugs is applied. Tricyclic antidepressant drugs are relatively well known together with selective serotonin reuptake inhibitors group. The aim of the study was to evaluate trazodone efficiency and safety in comparison to venlafaxine treatments of depressive episode, recurrent depressive disorders and depressive episode in bipolar disorders. MATERIAL AND METHOD: 115 patients were involved in the study. The research lasted 42 days. There were no essential differences between the control group of patients at the beginning of the study. RESULTS: The final result was 11.4 +/- 8.1 according to HAMD-S scale in trazodone group and 11.9 +/- 8.0 in venlafaxine group. Significant improvement evaluated in HAMD-S and CGI scale was observed in 61.4% patients trazodone treated and 59.4% in venlafaxine group. At the beginning of the treatment some patients suffered from unwanted symptoms. In venlafaxine group the most common were libido decrease up to 12.9% and gastro-intestinal dysfunction in 11.3%. In trazodone group the most common symptom was gastro-intestinal dysfunction in 5.6%. Due to severe unwanted symptoms the treatment was stopped in 12.9% patients venlafaxine treated and in 7.4% patients treated by trazodone. CONCLUSION: Our study showed similar efficiency and safety of trazodone and venlafaxine for depression disorders. Trazodone efficiency in comparison to venlafaxine was faster, especially in 14th study day. It suggests that trazodone characterized by potentially quicker beginning of activity in patients with depression disorders.

Adult↗
PubMed1983

Long-term therapy for depression with trazodone.

Trazodone and imipramine were compared in a two-center double-blind study of moderately to severely depressed outpatients. Results for 44 patients who have completed the 12-month comparison showed superior efficacy of trazodone at endpoint on all efficacy measures. Significant differences were also seen on individual Hamilton Depression Rating Scale items, with lower anxiety scores at 5 evaluation points for the trazodone group. Clinical Global Impressions ratings also favored trazodone treatment. Anticholinergic effects and tremor were significantly more frequent in imipramine-treated patients, whereas drowsiness was more frequent with trazodone. No significant changes were seen in blood pressure or ophthalmologic exams; 2 trazodone patients and 1 imipramine patient developed slight ECG changes during therapy; these may have been age-related. Continued clinical benefit has been seen in 12 patients who have received open-label trazodone for additional periods of up to 3 years. These findings show trazodone to be clearly effective in long-term treatment of moderate to severe depression; the drug may be of particular benefit when atropine side effects pose serious problems, as in the elderly and patients with cardiovascular disorders.

Ambulatory Care↗
PubMed1994

Comparison of bupropion and trazodone for the treatment of major depression.

Bupropion and trazodone were compared in a two-center, double-blind clinical trial of outpatients with moderate to severe major depression. After a 1-week placebo lead-in, 124 patients were randomly assigned to receive either bupropion (N = 63) or trazodone (N = 61) for 6 weeks; data from 111 patients were used in the efficacy analysis. Dosing ranged from 225 to 450 mg/day for bupropion and 150 to 400 mg/day for trazodone. The overall efficacy for each of the two drugs was similar; although improvement in the trazodone treatment group was significantly greater on day 7 because of the effects on sleep. At the end of treatment, 58% of the bupropion-treated patients and 46% of the trazodone-treated patients were considered much or very much improved. Weight measurements at the time of discontinuation indicated a 2.5-lb mean weight loss for the bupropion treatment group and a 1.2-lb mean weight gain for the trazodone treatment group. The adverse experience profiles for bupropion and trazodone were consistent with their known pharmacologic profiles (i.e., activating versus sedating). Anorexia and anxiety were reported significantly more often for the bupropion treatment group, whereas somnolence, appetite increase, and edema were reported significantly more often for the trazodone treatment group.

Adult↗
PubMed1989

Quantitative analysis of trazodone hydrochloride in tablets by an ion-selective electrode.

A simple assay procedure for the quantitation of trazodone hydrochloride in tablets, without prior separation, has been developed using a trazodone-selective electrode. The electrode was based on a trazodone:tetrakis(p-chlorophenyl)borate ion-pair complex, dioctyl phthalate, and polyvinyl chloride matrix that were mounted on a PTFE membrane. The electrode showed a near-Nernstian response in the range of 10(-2) to 5 x 10(-6) M trazodone over the pH range of 2.5 to 5.0, with a cationic slope of 58 mV/concentration decade. The durability of the electrode and the reproducibility of the performance among the electrodes were sufficient. The electrode was used for the determination of the pKa value of trazodone. The selectivity of the electrode to a number of interferences was investigated. Many inorganic cations (alkali and alkaline earth metals) and pharmaceutical excipients did not interfere, but some organic ammonium compounds interfered according to their extractability. Determination of 10 to 3000 micrograms/mL of trazodone hydrochloride in aqueous solution showed an average recovery of 100.6% (mean standard deviation 0.4%) by direct potentiometry. This assay was applied to determine trazodone hydrochloride in tablets and the results compared favorably with those obtained by high-performance liquid chromatography.

Chromatography, High Pressure Liquid↗
PubMed1982

The electrocardiographic and anticholinergic effects of trazodone and imipramine in man.

The electrocardiographic and anticholinergic effects of trazodone (150 mg) and imipramine (75 mg) were investigated in 8 healthy volunteers. Both agents increased the QTc interval and decreased T wave height, but the effects occurred earlier with trazodone (from 30 min onwards) than with imipramine (150 and 180 min after dosing). Both drugs decreased heart rate, imipramine at 30 and 60 min and trazodone at 90 min. After 120 min, heart rate began to increase with imipramine an effect which was not seen with trazodone. Salivary volume was significantly decreased by imipramine at 120 and 180 min whereas trazodone did not influence salivary volume. Plasma levels of trazodone and imipramine were significantly related to the decrease in T wave amplitude. The increase in QTc interval correlated significantly with the plasma level of imipramine. These results suggest that trazodone, like the tricyclic antidepressants prolongs ventricular repolarization; but, in contrast to imipramine, it does not have anticholinergic activity.

Adult↗
PubMed1997

Trazodone and triazolam: acute subject-rated and performance-impairing effects in healthy volunteers.

The present study compared the acute subject-rated and performance-impairing effects of trazodone and triazolam in seven healthy humans. Trazodone (50, 100 and 200 mg), triazolam (0.125, 0.25, 0.50 mg) and placebo were administered orally in a double-blind, crossover design. Drug effects were measured approximately 30 min before drug administration and repeatedly afterwards for 6 h. Trazodone and triazolam produced dose-related increases in subject-ratings of drug effect and sedation. The absolute magnitude of trazodone's and triazolam's effects was comparable across these measures, which suggests the doses tested were equivalent on some behavioral dimension. By contrast, triazolam, but not trazodone, increased subject ratings of "dizzy", "excited", "nervous", "restless", "stomach turning" and "itchy skin". Triazolam, but not trazodone, significantly impaired learning, recall and performance. The present findings suggest trazodone may be a viable alternative to benzodiazepine hypnotics like triazolam, especially when needing to minimize drug-induced impairment. Future research could extend the present findings by replicating them in a clinically relevant population such as individuals with histories of drug abuse.

Adult↗
PubMed1999

Trazodone and valproate in patients discontinuing long-term benzodiazepine therapy: effects on withdrawal symptoms and taper outcome.

Recent uncontrolled research suggested that trazodone and sodium valproate may be helpful in benzodiazepine (BZ) discontinuation. We therefore undertook a double-blind study to assess whether trazodone and valproate, as compared to placebo, would attenuate withdrawal and facilitate discontinuation in BZ-dependent patients with a minimum of 1 year daily BZ use. Seventy-eight patients, taking a mean dose of 19+/-17 mg/day of diazepam (or its equivalent), were stabilized for several weeks on their BZ (16 diazepam, 25 lorazepam, 37 alprazolam) and then for 1-2 weeks, pretreated with trazodone, sodium valproate or placebo before being tapered at 25% per week. All treatments were continued for 5 weeks post-taper. BZ-free status was assessed after 5 and 12 weeks post-taper. Neither trazodone nor valproate had any significant effect on withdrawal severity. Peak physician withdrawal checklist change from baseline to peak severity was 16.4 for trazodone, 18.04 sodium valproate and 18.24 placebo (F = 0.10; NS). Taper success rates were significantly effected by both active agents at the 5-week, but not 12-week, assessment. At 5 weeks post-taper, 79% of sodium valproate and 67% of trazodone, but only 31% of placebo patients were BZ-free (chi2 = 7.34; df 2; P<0.03). Major adverse events for trazodone were sedation and dry mouth, and for valproate, diarrhea, nausea and headaches.

Adult↗
PubMed1999

Acute behavioral effects and abuse potential of trazodone, zolpidem and triazolam in humans.

The present study examined the acute behavioral effects and abuse potential of three drugs commonly used to treat sleep disorders, trazodone, zolpidem and triazolam, and placebo in ten male volunteers with histories of alcohol and drug abuse. Trazodone (100, 200 and 300 mg), a triazolopyridine antidepressant, was included because antidepressants are being used more frequently to treat sleep disorders, but it is unclear whether they have a distinct behavioral pharmacologic profile relative to benzodiazepine hypnotics. Zolpidem (15, 30 and 45 mg), an imidazopyridine hypnotic, was tested because it is the most commonly prescribed hypnotic and purportedly has a unique benzodiazepine-receptor binding profile. Triazolam (0.25, 0.5 and 0.75 mg), a triazolobenzodiazepine hypnotic, was included as the standard component because previous laboratory studies have demonstrated that it has at least some abuse potential. Trazodone, zolpidem and triazolam generally produced comparable dose-related increases in scores on the PCAG scale of the ARCI, which suggests the doses tested were equivalent on some behavioral dimension. The effects of trazodone on subject-rated items thought to measure abuse potential (e.g., subject ratings of Willing to Take Again) were less than those observed with triazolam. Zolpidem and triazolam produced comparable effects on these measures. The highest dose of zolpidem, but not triazolam, increased ratings of Like Drug, Happy, Good Effects, Friendly, Elated, Carefree and Bad Effects. Triazolam and zolpidem produced dose-dependent impairment on all of the performance tasks. Trazodone impaired performance on some, but not all, of these tasks. Consistent with the pharmacokinetics of these compounds, the time-action functions of trazodone, zolpidem and triazolam were similar on these measures. These data suggest that trazodone has less abuse potential than triazolam, and may be a viable alternative to benzodiazepine hypnotics in individuals with histories of alcohol or drug abuse. By contrast, despite its unique neuropharmacological profile, the acute behavioral effects and abuse potential of zolpidem are comparable to those of triazolam.

Adult↗
PubMed1985

Trazodone and m-chlorophenylpiperazine. Concentration in brain and receptor activity in regions in the brain associated with anxiety.

Trazodone, its active metabolite 1-(m-chlorophenyl)piperazine (mCPP) and two isomers of mCPP were tested for affinity to the binding sites for [3H]flunitrazepam ([3H]FLU) and [3H]p-aminoclonidine ([3H]pAC) in the frontal cortex, amygdala and hippocampus of the rat. When tested at the binding site for [3H]flunitrazepam, trazodone showed an average IC50 of 1.7 mM in all three regions of the brain while mCPP yielded an average IC50 of 0.36 mM. These same two compounds, when tested at the binding site for [3H]p-aminoclonidine, resulted in an average IC50 of 4.5 microM for trazodone and 0.6 microM for mCPP. When plasma values of trazodone and mCPP in the rat were similar to those obtained in patients given therapeutic doses, the concentrations of trazodone were found to be between 6 and 7 microM and between 2 and 3 microM for mCPP in the same brain regions of the brain used in the binding assays. Thus, a sufficient concentration of trazodone and mCPP can accumulate in brain tissue to displace approx. 50% of the [3H]p-aminoclonidine from its binding site but very little [3H]flunitrazepam from its binding site. These results, combined with the reported anxiolytic effects of the alpha-2 agonist, clonidine and the noradrenergic hyperactivity theory of anxiety, indicate that the mechanism of the anxiolytic activity of trazodone, may be a direct action on the central alpha-2 binding site.

Animals↗
PubMed1989

Effects of repeated trazodone administrations on serotonergic neurotransmission: biochemical studies.

1. Repeated administrations of trazodone as well as imipramine or mianserin (10 mg/kg i.p. twice daily for 3 weeks) attenuated the norepinephrine (NE) stimulation of adenylate cyclase studied in brain minces. Therefore trazodone shares with "tricyclic" (imipramine) and "atypic" (mianserin) antidepressants the capability to modulate the beta-adrenergic function. 2. Daily treatments with imipramine or trazodone enhanced the Vmax of neural uptake of serotonin (5HT) in minces prepared from rat frontal cortex; in contrast mianserin failed to modify the [3H]-5HT uptake. 3. Repeated administrations of imipramine but not of trazodone or mianserin reduced the maximum number of [3H]-imipramine recognition sites which are located on serotonergic axon terminals. 4. Differently, only repeated administration of trazodone decreased Bmax values of [3H]-mianserin binding sites which are located on membranes innervated by serotonergic neurons. Moreover trazodone did not change the number or affinity of 5HT2 receptors either after single or repeated administrations; in contrast even a single administration with mianserin or repeated administrations with imipramine down-regulated [3H]-ketanserin specific binding in membranes prepared from the frontal cortex. 5. Our observations therefore suggest that trazodone, imipramine or mianserin exerts similar effects on the adenylate cyclase system, by acting on a interneuronal loop which links serotonergic and noradrenergic transmission function. However, its exact mechanism of action, in part resembling both tricyclic and atypic depressants, requires further examination.

Animals↗
PubMed2005

Effect of trazodone on hERG channel current and QT-interval.

Trazodone has been associated with prolonged QT-interval and increased risk of polymorphous ventricular tachycardias clinically and has demonstrated in vitro inhibition of hERG (human ether-á-go-go-related gene) channel current. This study attempts to put the effects of trazodone into perspective by comparing its hERG inhibition to that of three agents known to inhibit I(Kr), and comparing the effects of trazodone and cisapride on action potential duration and the QT-interval in the rabbit Langendorff heart preparation. Trazodone inhibited hERG channel current in a concentration-dependent manner with an IC50 of 0.69 microM. Like astemizole, terfenadine and cisapride, trazodone inhibits hERG channel current at clinically relevant concentrations. Like cisapride, trazodone increased both the QT-interval and APD90 in the Langendorff heart preparation in a reverse frequency-dependent manner at clinically relevant concentrations. These data strongly suggest that trazodone prolongs the QT-interval through inhibition of hERG channel current.

Action Potentials↗
PubMed2004

The effects of trazodone on sleep in patients treated with stimulant antidepressants.

BACKGROUND AND PURPOSE: To evaluate the effects of trazodone on subjective and objective measures of sleep in depressed insomnia patients treated with selective serotonin reuptake inhibitors (SSRIs). SSRIs can exacerbate or cause new insomnia while alleviating other symptoms of depression. Trazodone has been reported to be an effective hypnotic for patients with antidepressant-associated insomnia. PATIENTS AND METHODS: Twelve female patients were given either 100 mg trazodone or placebo for 7 days in a double-blind crossover design with a 7-day washout period. Polysomnographic recordings were repeated on the 3rd, 9th and 17th, 23rd nights after treatment with trazodone or placebo. Sleep was assessed by Pittsburgh sleep quality index (PSQI) at the beginning and end of the study. Psychological evaluation was done by Hamilton depression rating scale (HDRS). RESULTS: Trazodone significantly increased total sleep time, percentage of stages 3+4, sleep efficiency index, sleep continuity index and decreased percentage of stage 1, number of awakenings, stage shifts compared to the baseline. This improvement was also obtained after 7 days of treatment. The PSQI score was reduced to 5+/-1.6 at the end of the study. HDRS was reduced to 11.5+/-4.5 with trazodone and to 12.2+/-3 with placebo. CONCLUSION: Trazodone is effective in the treatment of antidepressant-associated insomnia.

Adult↗