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PubMed1979

A sensitive method for the simultaneous determination in biological fluids of imipramine and desipramine or clomipramine and N-desmethylclomipramine by gas chromatography mass spectrometry.

A procedure is described which permits the simultaneous determination of imipramine and desipramine or clomipramine and N-desmethylclomipramine in serum or plasma for concentrations in the range of 1-200 ng ml-1. Detection limits of 0.2 ng ml-1 for imipramine and 0.1 ng ml-1 for desipramine were demonstrated with a signal-to-noise ratio maintained at 2:1 or better. The method relies on the derivatization of the secondary amines with heptafluorobutyric anhydride and is based on the combined use of gas chromatography, electron impact mass spectrometry and computerized data handling. The assaying procedure is specific, accurate and precise. It is suitable for routine analyses and has sufficient sensitivity to permit monitoring the drug and metabolite levels in human plasma or serum resulting from a single therapeutic dose.

Chromatography, Gas↗
PubMed1986

Treatment of depression in chronic cocaine and phencyclidine abuse with desipramine.

An open field trial was conducted comparing desipramine and an active placebo in separate populations of chronic cocaine and phencyclidine (PCP) abusers, who discontinued their abuse. Subjects who received desipramine showed a decrease in depressive symptoms after a 20-40 day period regardless of whether they abused PCP or cocaine.

Adult↗
PubMed1979

High-performance liquid chromatographic assay for imipramine, desipramine, and their 2-hydroxylated metabolites.

High-performance liquid chromatographic method is presented for the simultaneous determination of imipramine, desipramine, and their 2-hydroxylated metabolites in plasma. The method involves a simple plasma extraction at basic pH with organic solvent, chromatography on a silica gel column, and fluorescence detection. Correlation with a GLC-mass spectrometric method for imipramine and desipramine is illustrated. The method can detect 1 ng of each component/ml of plasma, sufficient sensitivity for pharmocokinetic studies.

Chromatography, Gas↗
PubMed1981

Pharmacokinetic linearity of desipramine hydrochloride.

The pharmacokinetic linearity of two single oral doses of desipramine hydrochloride was examined in a parallel study involving 30 subjects. Fourteen subjects received 75 mg (3 x 25 mg) of desipramine hydrochloride, and 16 subjects received 150 mg (1 x 150 mg). An open one-compartment model with a lag time to the start of absorption was used to examine the pharmacokinetic linearity. The results of the study suggest that the kinetics are linear in the dose range studied.

Adult↗
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↗
PubMed1990

The involvement of desipramine-sensitive processes in the extraction of various catecholamines from plasma in the anaesthetized rabbit.

The effects of desipramine on the total body plasma clearance (Cl) as well as the systemic fractional extraction (ERs) of noradrenaline, dopamine, adrenaline, and isoprenaline, and on the pulmonary fractional extraction (ERp) of dopamine and adrenaline were determined in the anaesthetized rabbit. Under control conditions, noradrenaline, dopamine, adrenaline, and isoprenaline had Cl values of 59.5, 116.2, 68.0, 78.4 (ml kg-1 min-1) and ERs values of 0.709, 0.789, 0.694, 0.669, respectively. The ERp of dopamine was 0.235, while that of adrenaline did not differ from zero. Desipramine reduced the Cl of noradrenaline (by 20%), but did not affect that of the other amines. It also reduced the ERs of noradrenaline (by 31%), dopamine (by 10%) and adrenaline (by 10%); the ERp of dopamine was diminished by 84%.

Anesthesia↗
PubMed1988

Unaltered 5-HT- and desipramine-sensitive [3H]imipramine binding and [3H]5-HT uptake in rat brain after chronic imipramine and norzimeldine treatment.

Several reports have shown heterogeneity of [3H]imipramine binding to brain membranes. Recently, a high affinity and 5-HT sensitive [3H]imipramine binding site of protein nature, that was suggested to be identical to the substrate recognition site for 5-HT uptake, was demonstrated. Since most studies on the regulation of the [3H]imipramine binding sites by antidepressants have used desipramine displaceable binding, which is heterogenous in nature and contains binding not related to 5-HT uptake sites, the present report studies the possible effects of chronic (3 weeks) administration of imipramine or norzimeldine (10 mg/kg intraperitoneally twice daily) on 5-HT sensitive [3H]imipramine binding sites. For comparison, desipramine sensitive binding was also studied, as well as the physiological correlate 5-HT uptake. There were no changes in either [3H]imipramine binding or 5-HT uptake after the antidepressant treatment.

Animals↗
PubMed1976

Treatment of experimental imipramine and desipramine poisoning in the rat.

The influence of orally administered activated charcoal on organ concentrations of parenteral imipramine and desipramine was investigated. Ancillary distribution experiments indicated that the gastroenteral cycle of these substances might be more important than the enterohepatic cycle. Nevertheless the effectiveness of repeated activated charcoal dosage in lowering antidepressant concentrations of visceral organs is unpredictable. This is interpreted as a consequence of predominant binding of these drugs in the tissues, in contrast to drugs like acetosal and the barbiturates, which are distributed more evenly in the body water. The conclusion is, that activated charcoal has only limited value as an anitdotal adsorbent in imipramine or desipramine poisoning.

Adsorption↗
PubMed1982

The effect of repeated desipramine administration on water intake in rats.

Rats were maintained on a regimen of restricted access to water. Desipramine (DMI) IP 1 h prior to the access period dose-dependently reduced water intake. Following completion of the dose-response determination for the effect of desipramine or water intake, rats were divided into three groups for repeated administration. Rats in each group were injected both 1 h before and 15 min after the access period. The SAL-SAL group received saline both before and after the session, the DMI-SAL group received 10 mg/kg DMI before and saline after the session, and the SAL-DMI group received saline before and 10 mg/kg DMI after the session. Average water intake for rats in the DMI-SAL group decreased progressively during the first 5 days of repeated administration and then began to return toward baseline levels. Average water intake for rats in the SAL-DMI group decreased progressively from days 4-18 of repeated administration and then began to increase toward baseline levels. Rats repeatedly administered DMI (DMI-SAL and SAL-DMI groups) became tolerant to its effect on water intake, as indicated by a diminution of the DMI effect during repeated treatment and by a shift to the right in the DMI dose-response function after discontinuation of repeated DMI administration. Both groups of rats administered DMI repeatedly were less sensitive to amitriptyline-induced reduction of water intake than controls, thereby indicating the development of cross-tolerance to amitriptyline. Cross-tolerance to scopolamine did not develop. These findings demonstrate a behavioral effect of DMI that results in the development of tolerance. The lack of cross-tolerance to scopolamine suggests that tolerance development is not due to altered central cholinergic function.

Amitriptyline↗
PubMed1983

Relationship between plasma desipramine levels and clinical outcome for RDC major depressive inpatients.

Depressed patients (N = 31), who met Research Diagnostic Criteria for major affective disorder-depressed, were severely ill and maintained drug-free for a 1-week period on inpatient status. They received a fixed dose (150 mg/day) of desipramine for a 4-week period with drug plasma level determination and clinical ratings performed at fixed time intervals throughout the study. Despite these rigid criteria for entrance and clinical outcome measures, no obvious relationship between plasma desipramine level and clinical outcome was found. The clinical implications of this finding are discussed.

Adult↗
PubMed1984

The effect of imipramine and desipramine on mixed function oxidase in rats.

The effects of imipramine and desipramine on hepatic mixed function oxidase were measured in male Wistar rats. Both antidepressants increased hepatic cytochrome P-450 when given b.i.d. for 7 or 14 days. In vitro demethylation of imipramine was rather depressed than increased. 14CO2 exhalation from [N-methyl-14C] benzphetamine was increased by pretreatment with the antidepressants as well as with phenobarbital, but imipramine had no influence on the exhalation of the label from [6-methoxy-14C]- or [7-methoxy-14C]-scoparone. No difference was observed between treatment with imipramine or desipramine. It is concluded that changes of the demethylation rate of imipramine are not responsible for its delayed elimination observed after chronic treatment (Daniel et al. 1981).

Animals↗
PubMed1980

Differential effects of benztropine and desipramine on the high affinity uptake of paratyramine in slices of the caudate nucleus and hypothalamus.

The effect of benzotropine and desipramine on the uptake of dopamine and p-tyramine was studied in slices of caudate and hypothalamus. In the hypothalamus, of the various combinations of drugs and amines, desipramine inhibited p-tyramine uptake most effectively. In the caudate, benzotropine inhibited dopamine uptake most effectively. It is suggested that in the caudate, p-tyramine may possess its own unique transport system distinct from that utilized by dopamine which is inhibited by benzotropine.

Animals↗
PubMed1978

Effect of desipramine on the contents of some free amino acids of mouse brain.

I.p. injections of desipramine-HCl (100 mg/kg) produced decreases in the contents of several amino acids of mouse brain after 1 h. Using a 10-100 mg/kg range of doses, these effects appeared to be dose-dependent for alpha-alanine and aspartate. These changes may be due, in part, to a decrease in cerebral oxidative metabolism (Krebs cycle activity) which occurs secondarily to desipramine-induced hypothermia.

Amino Acids↗
PubMed1994

Post-stroke depression: combined treatment with imipramine or desipramine and mianserin. A controlled clinical study.

In a 6-week study the efficacy of combined treatment of imipramine plus mianserin was compared to combined treatment of desipramine plus mianserin in patients with post-stroke depression. Patients were required to have a minimum baseline total score of 15 on the 17-item Hamilton Depression Scale (HAMD). The Melancholia Scale (MES) was also used to measure severity of depressive states to show that somatic symptoms had little influence on the evaluation of depression. Out of 120 stroke patients screened, 20 patients fulfilled the inclusion criteria. The doses of the drugs were flexible, using side-effects as a guide during treatment. Both intention to treat analysis and efficacy data (excluding patients who had dropped out during the first 2 weeks of treatment) showed that imipramine (mean dose 75 mg daily) plus mianserin (mean dose 25 mg daily) was superior to desipramine (mean dose 66 mg daily) plus mianserin (27 mg daily). The MES was found to be more sensitive than the HAMD for measuring change in depressive states during treatment. The assessment of side-effects using the UKU scale showed good tolerance in general. The only difference between the two treatment groups was seen in micturition disturbances, where the imipramine treated patients had most complaints after 14 days of treatment, but the symptoms disappeared despite continuous treatment.

Aged↗
PubMed1990

Desipramine and restraint stress induce odor conditioned aversion in rats: suppression by repeated conditioning.

Rats exposed to one, three, or seven conditioning sessions defined by an olfactory conditioned stimulus and stress or antidepressant administration as unconditioned stimulus were later tested for their preference for the conditioned olfactory stimulus. A significant reduction of the time spent in the conditioned stimulus was observed in animals exposed to one and three pairings with stress or three pairings with desipramine. A lack of conditioned aversion was observed in animals exposed to seven pairings with either reinforcer. These data could indicate that the adaptative mechanisms elicited by repeated stress or desipramine may be involved in the decrease of conditioned aversion.

Animals↗
PubMed1989

Effect of an inhibitor of noradrenaline uptake, desipramine, on cell proliferation in the intestinal crypt epithelium.

The intestinal mucosa receives an adrenergic innervation for which there is no commonly accepted function. However, in recent years, cell kinetic studies have raised the possibility that this innervation may be an important regulator of crypt cell proliferation. The effects of noradrenaline released from adrenergic nerves is terminated principally by re-uptake of the amine into the nerve and this process can be inhibited by the antidepressant drug, desipramine. In this report desipramine is shown to accelerate crypt cell proliferation in intact, but not in chemically sympathectomized rats, thus adding support to the notion that regulation of crypt cell division is an important function of the sympathetic nervous system.

Animals↗
PubMed1999

Comparison of the effects of venlafaxine, paroxetine and desipramine on the pupillary light reflex in man.

RATIONALE: The time-course of the pupillary light reflex response is determined by the successive activation of the parasympathetic and sympathetic innervations of the iris, the latency and the amplitude reflecting parasympathetic and the recovery time mainly sympathetic activity. OBJECTIVE: To compare the effects of single doses of three antidepressants (venlafaxine: serotonin/noradrenaline reuptake inhibitor, paroxetine: selective serotonin reuptake inhibitor, and desipramine: tricyclic antidepressant) on resting pupil diameter and the pupillary light reflex response. METHODS: Fifteen healthy male volunteers participated in five weekly sessions, each of which was associated with one treatment (venlafaxine 75 mg or 150 mg, paroxetine 20 mg, desipramine 100 mg, or placebo) according to a double-blind, double-dummy, balanced, cross-over design. An infrared binocular television pupillometer was used for the recording of the resting pupil diameter and the pupillary light reflex in darkness, in previously dark-adapted eyes. Resting pupil diameter in darkness was recorded before and after treatment. The pupillary light reflex was elicited after treatment, with six light flashes (green, 565 nm peak wavelength) of 200 ms duration and of incremental illuminance (measured in the plane of the cornea): 3.0 x 10(-3) 8.5 x 10(-3) 2.5 x 10(-2), 7.0 x 10(-2), 0.18, 0.43 mW cm(-2). The parameters studied were: latency, amplitude and 75% recovery time. RESULTS: Analyses of variance followed by post hoc tests (least significant difference test or Dunnett's test; P < 0.05) revealed that both doses of venlafaxine produced a significant increase in resting pupil diameter, decrease in amplitude and shortening of the 75% recovery time of the light reflex response; venlafaxine 150 mg prolonged the latency, while the other treatments had no significant effects. CONCLUSIONS: The increase in resting pupil diameter could be indicative of parasympathetic inhibition and/or sympathetic activation. The shortening of the recovery time of the light reflex response is consistent with sympathetic potentiation resulting from noradrenaline uptake blockade in the iris. The prolongation of the latency and decrease of the amplitude of the light reflex response are indicative of a parasympatholytic effect of venlafaxine. However, as venlafaxine has negligible affinity for muscarinic cholinoceptors, this effect cannot be attributed to the blockade of cholinoceptors in the iris. A possible explanation for this finding is that it reflects a central rather than a peripheral effect of the drug: the blockade of noradrenaline uptake in the brain could lead to the potentiation of the noradrenergic inhibition of central parasympathetic (Edinger-Westphal) neurones. These results demonstrate the ability of therapeutically relevant single doses of venlafaxine to potentiate noradrenergic responses in man, consistent with the blockade of noradrenaline uptake.

Adrenergic Uptake Inhibitors↗