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At least 1,423 records · Page 79Linked to original sources
PubMed1991

Effects of tetrodotoxin and imipramine on the cardiac responses to nicotine in isolated, blood-perfused canine heart preparations.

The effects of nicotine on the sinus rate and atrial or left ventricular contractile force were investigated in the isolated, blood-perfused dog right atrium and left ventricle. Nicotine (3-300 nmol) in the right atrium induced dose-dependent negative followed by positive chronotropic and inotropic responses, whereas nicotine caused only a positive inotropic response in the left ventricle. The negative responses to nicotine were blocked by atropine, hexamethonium (C6), and tetrodotoxin (TTX). The positive effects of nicotine were abolished by propranolol and C6. TTX significantly inhibited the positive responses to nicotine by about 50% in the atrial preparation and totally suppressed them in the left ventricle. Imipramine inhibited the positive cardiac responses to nicotine and tyramine, but potentiated the responses to noradrenaline (NA) in atrial and ventricular preparations. These results suggest that (a) nicotine induces negative and positive cardiac effects mediated by parasympathetic ganglionic nicotinic receptors and presynaptic nicotinic receptors of the postganglionic sympathetic nerves, respectively, in the dog heart; (b) there are few parasympathetic ganglionic cells in the dog left ventricle; (c) the positive cardiac responses to nicotine are caused by both TTX-sensitive and TTX-insensitive NA release mechanisms; and (d) imipramine inhibits the positive cardiac responses to nicotine at the presynaptic nicotinic receptor sites of the postganglionic sympathetic nerves.

Animals↗
PubMed2003

A comparison of drug effects in latent inhibition and the forced swim test differentiates between the typical antipsychotic haloperidol, the atypical antipsychotics clozapine and olanzapine, and the antidepressants imipramine and paroxetine.

Current animal models of antipsychotic activity that have the capacity to dissociate between typical and atypical antipsychotic drugs (APDs) have two drawbacks: they require previous administration of a psychotomimetic drug, and they achieve the dissociation by demonstrating effectiveness of atypical but not typical APDs, thus losing specificity and selectivity for APDs. The present experiments were designed to solve these problems by using two non-pharmacological tests: latent inhibition (LI), in which potentiation of the deleterious effects of non-reinforced stimulus pre-exposure on its subsequent conditioning served as a behavioral index for a common action of typical and atypical APDs (antipsychotic), and the forced swim test (FST), in which reduction of immobility served as a behavioral index for a dissimilar action of these drugs (antidepressant). The typical APD haloperidol (0.1 mg/kg), the atypical APDs clozapine (2.5 mg/kg) and olanzapine (0.6 mg/kg), and the antidepressants imipramine (10 mg/kg) and paroxetine (7.0 mg/kg), produced distinct patterns of action in the two tests: haloperidol potentiated LI and increased immobility in the FST, clozapine and olanzapine potentiated LI and decreased immobility in the FST, and imipramine and paroxetine decreased immobility in the FST and did not potentiate LI. Thus, the comparison of drug effects in LI and FST enabled a discrimination between typical and atypical APDs without losing selectivity for APDs.

Animals↗
PubMed1977

Controlled randomized group comparison of nomifensine and imipramine in depressive illness.

1. Nomifensine, an isoquinoline dopaminergic agonist, was investigated in a randomized double-blind group comparison with imipramine, in 40 out-patients with depression. 2. Assessments were made at weekly intervals for 4 weeks using the Hamilton Depression Scale and the Beck Depression Inventory. Blood, kidney and liver function were also monitored weekly. 3. Nomifensine was shown to be at least as effective as imipramine in relieving depression and to relieve tha anxiety component of the disease significantly more rapidly. Neither drug produced serious unwanted effects.

Adult↗
PubMed1992

Dosage optimization methods applied to imipramine and desipramine in enuresis treatment.

Three methods for estimating maintenance dosage requirements of imipramine were compared retrospectively in 146 enuretic patients. The dosing methods evaluated included individual (serum levels data) and/or population (average pharmacokinetic parameter) information. The use of imipramine and desipramine serum concentrations, as opposed to average population parameters only, improved forecast precision and accuracy for dosage individualization. The clinical acceptability of this was achieved through knowledge of a single serum concentration. No significant differences were seen between non-linear regression and the Bayesian method, this is in agreement with the high contribution of the patient's data to the Bayesian fitting (FF = 0.8). When one or two serum level data were available, a better performance was obtained by estimating pharmacokinetic parameters than level:dose ratios.

Adolescent↗
PubMed1982

The action of imipramine on the lower urinary tract of the dog.

Imipramine at 1 mg/kg body weight reduced contractions of the urethra and bladder produced in response to pelvic nerve stimulation by 58 and 56% in female anaesthetised dogs. Responses to injection into the internal iliac artery of acetylcholine, histamine and 5 hydroxytryptamine (5HT) were also reduced but those to ATP and noradrenaline were not altered. Atropine (0.1 mg/kg) blocked responses to acetylcholine and pelvic nerve stimulation but was without action on responses to ATP, histamine or 5HT. Mepyramine (1 mg/kg) but not metiamide (0.5 mg/kg) selectively blocked responses to histamine. The responses to pelvic nerve stimulation or acetylcholine were not altered. It was concluded that imipramine does not have significant anticholinergic action and is unlikely to block uptake of biogenic amines. The powerful inhibitory action on histamine responses could reduce the effects of circulating histamine but cannot explain the reduction of the nerve-induced response.

Animals↗
PubMed1983

High- and low-affinity binding of [3H]imipramine in mouse cerebral cortex.

Binding of [3H]imipramine in mouse cerebral cortex was found to be nonhomogeneous. Competition experiments, Scatchard analysis, and Hill plots are compatible with the existence of binding with high (nanomolar) and low (micromolar) affinity. Low-affinity binding could be eliminated by the use of low concentrations of imipramine as the competing ligand. In contrast to the high-affinity binding, the low-affinity binding was found to be unrelated to the neuronal uptake system for serotonin.

Animals↗
PubMed1969

The interactions of noradnamine and imipramine-like antidepressant drugs.

1. The hypothesis of Roberts & Broadley (1965) that noradnamine formation in the brain is responsible for endogenous depression has been investigated in mice.2. Injections of noradnamine given directly into the lateral ventricles caused convulsions and profound hypothermia, but were without effect if given subcutaneously.3. The hypothermia, but not the convulsions, induced by noradnamine was reversed by imipramine-like antidepressant drugs given before or after the injection of noradnamine. The convulsions but not the hypothermia were abolished by phenobarbitone.4. Increasing doses of nortriptyline produced a parallel shift of the hypothermic log dose-response curve for intraventricular injections of noradnamine to the right.5 The minimal effective dose of nortriptyline required to reverse noradnamine hypothermia was the same whether the nortriptyline was injected directly into the lateral ventricle or subcutaneously.6. No evidence was found to substantiate the claim that reserpine hypothermia is mediated by noradnamine formation in the brain.7. Intraventricular, but not intraperitoneal, injection of noradnamine caused a depletion of brain noradrenaline and an increase in brain 5-hydroxytryptamine. These changes did not result from the convulsive activity and were not modified by pretreatment with nortriptyline. No effect on heart noradrenaline levels was recorded.8. Noradrenaline, given subcutaneously, also antagonized the hypothermic response to noradnamine.9. The reversal of noradnamine hypothermia by both noradrenaline given subcutaneously and nortriptyline was blocked by alpha and beta-adrenoceptive receptor blocking agents.10. It is considered that the mode of action of the antagonism of noradnamine hypothermia by imipramine-like antidepressant drugs is a peripheral and not a central mechanism and probably results from a potentiation of the effects of circulating noradrenaline released by noradnamine.

Animals↗
PubMed1973

Role of brain monoamines in the fatal hyperthermia induced by pethidine or imipramine in rabbits pretreated with a monoamine oxidase inhibitor.

1. The intravenous infusion of pethidine or imipramine, in doses of 5 mg/kg, caused fatal hyperpyrexia in rabbits premedicated with pargyline.2. The drug interaction was not antagonized when either reserpine or alpha-methyl-p-tyrosine were administered with pargyline. Neither reserpine nor alpha-methyl-p-tyrosine prevented the rise in brain stem 5-hydroxytryptamine content following monoamine oxidase inhibition, although the increase in catecholamines normally produced by pargyline was prevented.3. The development of fatal hyperthermia was completely prevented when rabbits were treated with p-chlorophenylalanine prior to pargyline premedication. In these animals, the concentration of brain stem catecholamines, but not 5-hydroxytryptamine, was increased.4. The results indicate that the hyperthermia evoked by pethidine or imipramine in combination with monoamine oxidase inhibitors can take place only in the presence of raised concentrations of 5-hydroxytryptamine in the brain stem.

Amines↗
PubMed1987

Long-term imipramine treatment enhances locomotor and food intake suppressant effects of m-chlorophenylpiperazine in rats.

1 Administration of the 5-HT1B receptor agonist m-chlorophenylpiperazine (m-CPP) to rats produces dose-dependent decreases in locomotor activity and food intake. 2 The locomotor suppressant effect of m-CPP was inhibited by the 5-hydroxytryptaminergic antagonist, metergoline, but not by phentolamine, propranolol, clonidine, or haloperidol. 3 The locomotor suppressant effects of m-CPP were enhanced following long-term (but not short-term) treatment with imipramine, possibly reflecting the postulated development of a functional supersensitivity of 5-HT1B receptors mediating locomotion during longer-term antidepressant drug treatment. 4 The food intake suppressant effects of m-CPP were enhanced following both short (3-5 days) and longer-term (21 days) treatment with imipramine. Rapidly developing 5-hydroxytryptamine uptake inhibition may be responsible for this change, or it may represent an earlier adaptive change in the 5-HT1B receptors mediating food intake compared to more complexly modulated motor responses.

Animals↗
PubMed1987

Treatment of the unstable bladder with propantheline and imipramine.

This study shows propantheline and imipramine to be effective in the management of the unstable bladder. It emphasizes the need for urodynamic studies for the accurate diagnosis of urinary incontinence. Comparisons have been made of the efficacy of propantheline and imipramine in various groups of incontinent women and indicates that in appropriately selected groups the 'cure' rate is over 70% but if sphincter weakness is excluded, urodynamics cannot differentiate between those women with unstable bladders who will respond to this medication and those who will not.

Drug Therapy, Combination↗
PubMed1979

Comparison of Vivalan (viloxazine hydrochloride) with imipramine in the treatment of depression. A double-blind study.

Twenty-eight hospitalized patients with depressive illness entered a double-blind trial to compare viloxazine hydrochloride (Vivalan) with imipramine. Both drugs produced a statistically significant improvement in the depressive symptoms as early as the 7th day, measured by the HRS. A side effects check-list showed no significant difference between Vivalan and imipramine. A lack of anticholinergic effects was noted in the Vivalan group although upper gastro-intestinal side effects were more frequent. Two patients in the Vivalan group withdrew due to gastric symptoms.

Adjustment Disorders↗
PubMed1986

Effect of a selective serotonin uptake inhibitor in agoraphobia with panic attacks. A double-blind comparison of zimeldine, imipramine and placebo.

A double-blind clinical trial of zimeldine, a potent inhibitor of central serotonin reuptake, versus imipramine and placebo was carried out on 44 patients suffering from agoraphobia with panic attacks. Zimeldine was a superior treatment on all rating scales other than a global rating scale which did not reach statistically significant superiority. Imipramine was not shown to be superior to placebo. The implications of these results for further research on the underlying pathophysiology of agoraphobia with panic attacks are discussed.

Adult↗
PubMed1986

3-MHPG as a non-predictor of antidepressant response to imipramine and electroconvulsive therapy.

The urinary excretion of 3-methoxy, 4-hydroxyphenyl-glycol, (3-MHPG) was measured in 20 unipolar depressed patients before treatment with imipramine and electroconvulsive therapy (ECT) to investigate the relationship between pretreatment urinary excretion of 3-MHPG and clinical response. There was no difference in 3-MHPG excretion for depressed patients and controls. There was no significant difference between the mean percentage reduction of Hamilton Depression Rating Scale Scores in "low" and "high" excretors of 3-MHPG in the imipramine and ECT group of patients after four weeks of treatment.

Adult↗
PubMed1988

Does 3H-imipramine binding asymmetry indicate psychiatric illness?

We have accepted that serotonin is essentially an inhibitory neurotransmitter in the human brain, so we propose that it is precisely this inhibiting effect that has weakened in psychiatric cases. We have investigated the asymmetry of tritiated imipramine binding sites (Bmax) in the frontal cortices of homicide victims (n = 6) and controls (n = 6) who died of natural causes. Of these homicide victims examined in our experiment, five proved to have been psychiatric cases and one case had no psychiatric record. The two groups were comparable in age, gender and postmortem delay. The number of imipramine binding sites (Bmax) in the frontal cortices of controls was significantly higher in the right hemisphere than in the left hemisphere. But the homicide victims who were psychiatric cases had significantly higher (Bmax) values in the left hemisphere. While we only found higher Bmax values in the left hemisphere of homicide victims with mental diseases, our data may serve to prove the direct role of the serotonergic mechanism in the development of psychiatric cases.

Brain↗
PubMed1988

Adrenoceptor and imipramine receptor binding during the menstrual cycle.

The binding characteristics of platelet alpha 2-adrenoceptors, lymphocyte beta 2-adrenoceptors and platelet imipramine receptors were studied in five women during their menstrual cycle. A significant cyclic variation in the number of beta 2-adrenoceptor sites on intact lymphocytes was found during the menstrual cycle, while binding to alpha 2-adrenoceptors and imipramine receptors remained unchanged.

Adult↗
PubMed1988

Imipramine binding in depression and other psychiatric conditions.

30 studies of platelet 3H-imipramine binding in depressed patients are reviewed. 19 of these studies found that depressed patients had lower binding than control persons, whereas 11 studies found no difference. This discrepancy is discussed and it is concluded that methodological problems may account for a substantial part of the low imipramine binding in depressed patients.

Blood Platelets↗
PubMed1990

Platelet tritiated imipramine binding in psychiatric patients: relationship to symptoms and severity of depression.

The clinical and research significance of reduced imipramine binding has remained unclear despite considerable investigation. This study used an assay of demonstrated reliability to investigate the clinical correlates of imipramine binding to platelets in 63 depressed and 33 nondepressed psychiatric patients and 40 healthy control subjects. Both patient groups had Bmax values significantly lower than those of the healthy controls. Unequivocal associations between binding parameters and individual symptoms or groups of symptoms were not established, but a negative correlation between Kd and the number of adverse life events experienced in the preceding 6 months was apparent. These findings provide no support for the view that reduced binding is a trait marker for susceptibility to depression and cast doubt on its specificity as a state marker for the syndrome of depression.

Adult↗
PubMed1991

Platelet imipramine binding and serotonin uptake in obsessive-compulsive patients.

Platelet imipramine binding was measured in 16 drug-free nondepressed patients (aged 20-61 years, mean +/- SD 35 +/- 8) suffering from obsessive-compulsive disorder (OCD) and in 16 sex-, race- and age-matched healthy controls. Imipramine binding capacity and affinity were not different in the 2 groups. Platelet serotonin (5-HT) uptake capacity, Vmax, was also measured in 15 of these patients and their matched controls. Vmax was significantly higher in the patients (309 +/- 149 pmol/10(9) cells/min) than in the controls (181 +/- 110). An increase in platelet 5-HT uptake supports the involvement of 5-HT in OCD and may suggest that a hyperactive serotonergic system is present in this disorder.

Adult↗