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At least 613 records · Page 34Linked to original sources
PubMed1986

Quantitative homogeneous enzyme immunoassays for amitriptyline, nortriptyline, imipramine, and desipramine.

We describe specific EMIT homogeneous enzyme immunoassays for amitriptyline, nortriptyline, imipramine, and desipramine in patients' serum samples. Before analysis, an easily performed extraction step involving the use of 500 microL of sample and a 1-mL disposable column eliminates cross-reacting polar metabolites. The range of the standard curve for the first three drugs is 25 to 250 micrograms/L, and for desipramine is 50 to 500 micrograms/L. Within-run and between-run CVs are less than 10% throughout the range of the assays. Results for patients' samples obtained by this method and by "high-performance" liquid chromatography compare well, showing a slope range of 0.94-1.04 and correlation coefficients ranging from 0.93 to 0.96, depending on the assay.

Amitriptyline↗
PubMed1987

Testicular swelling associated with desipramine.

Two cases of testicular swelling associated with desipramine therapy are described. In one case, the swelling resolved with discontinuation of desipramine; in the other, the swelling subsided despite continuation and an increase in dose. These cases may represent a local variant of angioneurotic edema; however, further study is required to determine the exact etiologic mechanism.

Adult↗
PubMed1985

Nonlinear desipramine pharmacokinetics: a case study.

A case of nonlinear desipramine pharmacokinetics is described. During routine clinical monitoring serum desipramine concentrations appeared to change disproportionately with dose. Following a series of controlled dosage decreases, from 400 to 50 mg/day, the patient's steady state serum concentrations fit a nonlinear pharmacokinetic model. This curvilinear serum concentration-dose relationship suggests saturation of hepatic metabolism and signals the need for caution when predicting or titrating doses against serum drug concentrations. The implications of this new finding are discussed.

Aged↗
PubMed1980

[Changes of neuronal activity in the rat's hippocampus under long-term treatment with desipramine].

Long-term treatment of rats with the antidepressive desipramine increase in the hippocampus the number of neurons with low spontaneous discharges and affects the animals' response to microiontophoretically applied noradrenalin. Additional acute administration of desipramine causes, after long-term treatment with the antidepressive, a stronger increase in noradrenalin induced inhibition of the firing rates as compared with controls.

Action Potentials↗
PubMed1984

Antidepressants in concomitant chronic back pain and depression: doxepin and desipramine compared.

Doxepin and desipramine at final doses of 188 and 173 mg/day, respectively, were compared in 36 volunteers with major affective or dysthymic disorder and chronic back pain. Both drugs produced significant decreases in depression, with an overall response rate of 70%; no significant difference was seen between groups. Pain ratings also decreased significantly in both groups (overall response rate = 50%); pain severity showed a better response to doxepin than to desipramine. While baseline pain, depression, and anxiety were correlated, treatment changes in these measures did not correlate. CSF beta-endorphin levels did not change with treatment. The usefulness of an antidepressant with anxiolytic properties, such as doxepin, is discussed.

Adult↗
PubMed1984

Treatment of outpatients with desipramine.

Marginal differences in adverse effects become the basis of selection among equally effective drugs, especially in outpatient treatment. Desipramine's side effect profile makes it a particularly acceptable drug for the outpatient treatment of depression or depression with panic attacks. Relevant aspects of desipramine's pharmacologic properties and of prescribing practices are reviewed.

Ambulatory Care↗
PubMed1984

Desipramine: an overview.

It is proposed that factors including a long "track record," perceived lack of anticholinergic effects, suggestions of earlier onset of action, and the concept of noradrenergic specificity have contributed to the widespread clinical use of desipramine. Recent studies bearing on these clinical beliefs are reviewed, with a focus on desipramine side effects, specificity, and speed of onset as compared to other tricyclics and to new generation antidepressants.

Clinical Trials as Topic↗
PubMed1984

Relationship of desipramine plasma levels to therapeutic response: a critical reappraisal of the data.

The literature on the relationship between desipramine plasma levels and therapeutic response is reviewed. Although no clear pattern has emerged from the available studies, the data suggest that plasma levels of 125 ng/ml should be attained before moderately to severely ill patients are considered nonresponsive to desipramine. An upper therapeutic plasma level of 170 ng/ml may exist for patients with less severe illness. Future studies should control for severity of illness in assessing dose-response relationships.

Ambulatory Care↗
PubMed1983

Cocaine and amphetamine dependence treated with desipramine.

Desipramine was administered to 8 amphetamine- and 14 cocaine-dependent persons to assist withdrawal. Nineteen of 22 (86.4%) reported discontinuation of drug use within two to seven days, of which 15 (68.2%) gave urine samples negative for amphetamines or cocaine. Recent primate studies show that chronic methamphetamine administration markedly depletes brain norepinephrine, which suggests that desipramine is probably effective in treating amphetamine and cocaine dependency because it selectively blocks norepinephrine uptake.

Adult↗
PubMed1983

[Effect of desipramine and social isolation on neuronal activity in rat hippocampus].

Chronic treatment of rats with desipramine leads to an increase of hippocampal neurons with low spontaneous activity. After an isolation rearing period of three months an increased spontaneous activity is seen in the hippocampus of rats. Furthermore the hippocampal spontaneous activity is related to age. Opposite alterations of spontaneous activity in desipramine treated and socially isolated rats, respectively, as well as their relations to noradrenergic transmission processes are discussed. The isolation syndrome as a model to test substances with antidepressive properties is also reviewed.

Animals↗
PubMed1983

Anorgasmia associated with imipramine but not desipramine: case report.

A case of imipramine-induced orgasmic inhibition in a woman is reported. Desipramine, the metabolite of imipramine, did not produce this reaction. The ability of imipramine to block the CNS neuronal reuptake of serotonin (a property not shared by desipramine) is considered the probable pathophysiologic mechanism in the failure to achieve orgasm.

Desipramine↗
PubMed1984

Effects of chronic desipramine on plasma norepinephrine concentrations and cardiovascular parameters in elderly depressed women: a preliminary report.

The effect of chronic administration of desipramine, a relatively specific inhibitor of the reuptake of norepinephrine (NE), on heart rate, blood pressure, and concentrations of NE in plasma was examined in elderly depressed women. Plasma NE concentrations rose significantly following administration of desipramine, while there was no significant change in either heart rate or blood pressure. Implications of these findings are discussed with relationship to the selection of appropriate types and doses of antidepressants in the elderly.

Aged↗
PubMed1978

Imipramine and desipramine plasma levels: relationship to dosage schedule and sampling time.

Tricyclic antidepressant plasma levels were determined after administration if imipramine (11 patients) and desipramine (ten patients) as a single daily bedtime dose or in divided doses. Plasma levels of the tricyclics were relatively stable on both dosage schedules due to the long plasma half-lives of these drugs. No difference was found between the two dosage schedules and the therapeutic effectiveness or the severity of side effects. The majority of patients preferred the single dose schedule. These findings support the use of a single daily dose of imipramine and desipramine.

Adult↗
PubMed1982

Estimating steady state desipramine levels in noninstitutionalized elderly patients using single dose disposition parameters.

Clearances calculated from single oral dose data have been utilized to predict steady state levels of desipramine in 12 noninstitutionalized depressed elderly patients. Observed steady state plasma levels correlated very well (r = 0.967, p less than 0.0005) with those predicted from single dose clearances, but not with plasma levels obtained 20 hours after a single oral dose (r = 0.24, p greater than 0.2). The mean half-life of desipramine (20.9 hours) in this group of elderly (mean age, 72 years) was considerably less than values of "apparent disappearance" half-life previously reported for elderly patients receiving imipramine. The single dose clearance technique yielded a precise criterion for quantitating early compliance with and adjusting drug dosing regimens.

Aged↗
PubMed1994

Cyclic AMP and inositol phosphate accumulations in rat brain cortical slices following chronic citalopram or desipramine administration.

The influence of chronic administration of desipramine (16 mg/kg per day for 8 days) or citalopram (1 mg/kg per day for 8 days) on the serotonergic and noradrenergic stimulations of phosphoinositide hydrolysis and cyclic AMP formation was investigated in rat cerebral cortical slices. This was done by means of a prelabelling method allowing the simultaneous measurement of the accumulations of (3H) inositol phosphates ((3H)IP) and of (14C) cyclic AMP. Our results show that neither of the two drugs altered the inhibition of adenylate cyclase activity induced by serotonin1 (5-HT1) receptor agonists nor did they alter 5-HT1A and 5-HT1B receptor densities. Similarly they did not modify the stimulation of the inositol phosphate metabolism induced by 5-HT or norepinephrine (NE). Desipramine treatment decreased both beta-adrenoceptor-elicited cyclic AMP accumulation (-37%) and beta-adrenoceptor density (-29%), whereas citalopram was without effect. These results reinforce the idea that the ability of antidepressants to decrease the activity of the beta-adrenoceptor-adenylate cyclase complex is not common to all antidepressants, and provide no evidence for the involvement of 5-HT1A and/or 5-HT1B in the mechanism of action of these drugs.

Animals↗
PubMed1994

Inhibition of desipramine hydroxylation in vitro by serotonin-reuptake-inhibitor antidepressants, and by quinidine and ketoconazole: a model system to predict drug interactions in vivo.

Biotransformation of the tricyclic antidepressant desipramine (DMI) to its metabolite 2-hydroxy-desipramine (2-OH-DMI) was studied in vitro using microsomal preparations from human, monkey, mouse and rat liver. In all species 2-OH-DMI was the principal identified metabolite. Mean (+/- S.E.) reaction parameters in six human liver samples were: Vmax, 0.11 +/- .02 nmol/ml/min/mg protein; Km, 16.1 +/- 4.2 microM. Quinidine was a highly potent inhibitor of 2-OH-DMI formation (mean Ki = 0.053 microM), consistent with the presumed role of Cytochrome P450-2D6 in mediating this reaction. Ketoconazole was a much less potent inhibitor (mean Ki = 10.3 microM). Two serotonin-specific reuptake inhibitor (SSRI) antidepressants, and their respective metabolites, were evaluated as potential inhibitors of 2-OH-DMI formation. Fluoxetine (FLU) and norfluoxetine (NOR) were the most potent inhibitors (mean Ki values: 3.0 and 3.5 microM, respectively). Sertraline (SERT) and its metabolite desmethylsertraline (DES) also inhibited the reaction (mean Ki: 22.7 and 16.0 microM), but were significantly less potent than FLU or NOR. Values of Ki and Km measured in vitro were used to generate a theoretical prediction of the degree of clearance inhibition in vivo at any given concentration of substrate and inhibitor. The model was applied to a clinical study in which DMI clearance in humans was impaired by coadministration of FLU (yielding FLU and NOR in plasma) or by SERT (yielding SERT and DES in plasma). Use of plasma SSRI concentrations in the predictive model underestimated the actual impairment of DMI clearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Desipramine-induced blue-gray photosensitive pigmentation.

BACKGROUND: Blue-gray pigmentation of the skin can be elicited by several medications. We report the first case (to our knowledge) of desipramine-induced photosensitive blue-gray pigmentation. OBSERVATIONS: Diffuse blue-gray pigmentation on sun-exposed surfaces was noted in a healthy 48-year-old woman who had been taking desipramine hydrochloride for 8 years. Ultrastructural studies demonstrated the presence of melanin and homogeneous electron-dense material in the dermis. CONCLUSIONS: We conclude that tricyclic antidepressant agents represent another class of medications responsible for blue-gray cutaneous pigmentation.

Desipramine↗