Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pimozide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

Phase II trial of the dopaminergic inhibitor pimozide in previously treated melanoma patients.

Pimozide, a potent neuroleptic which inhibits the release of pituitary releasing factors and is an effective dopamine antagonist, was administered to 30 patients with previously treated metastatic melanoma. Six patients were inevaluable because of poor drug tolerance (two), disease progression within 1 week and death within 2 weeks (three), and death from other causes (one). Among the 24 evaluable patients, two had complete response, two had partial response, and two had disease stabilization. Responses were observed in soft tissue, lymph nodes, liver, and lung. Toxic effects consisted of extrapyramidal manifestations in nine patients and malaise in seven. Pimozide has activity in patients with previously treated metastatic melanoma (17% response rate in evaluable patients) and merits consideration of further study in combination regimens.

Adult↗
PubMed1980

Effects of dopamine, apomorphine gamma-hydroxybutyric acid, haloperidol and pimozide on reflex bradycardia in rats.

The cardiovascular responses to i.v. doses of epinephrine were assessed in vehicle-controlled, dopamine-treated, apomorphine-treated, gamma-hydroxybutyric acid-treated, haloperidol-treated and pimozide-treated rats, under urethan anesthesia. Previous exposure to several injections of epinephrine did not change the basal values of arterial pressure and heart rate. It was found that dopaminergic transmission alterations within the brain did produce some influence on the reflex bradycardia in response to an elevation in arterial pressure. Blockade of dopaminergic receptors in brain with either haloperidol or pimozide produced a significant recution in reflex bradycardia compared to the controls. In contrast, either direct activation of central dopamine receptors witth dopamine and apomorphine or indirect activation of central dopamine receptors with gamma-hydroxybutyric acid led to an enhancement in epinephrine-induced bradycardia. The data indicate that central dopmaine systems play a role in the elaboration or modulation of reflex bradycardia. Specifically, brain dopamine appears to facilitate reflex bradycardia since activation of dopamine systems facilitated and blockade inhibited reflex bradycardia.

Animals↗
PubMed1993

[Pimozide in the treatment of psychogenic eating disorders].

PIMOZIDE was given to 14 pat. with anorexia nervosa and 21 pat. with bulimia nervosa The drug evaluated positively some symptoms of eating disorders. Most significantly it improved the bulimic episodes and purging. The accompanying psychiatric symptomatology (depression and anxiety) was mostly not improved. We conclude that Pimozide may be a useful medication in the therapy of basic symptoms (bulimia, purging) in bulimic forms of eating disorders.

Adolescent↗
PubMedDate not supplied

Pimozide (Orap) in patients with pseudo-neurotic behaviour.

Pimozide 2-12 mg (median 4 mg) was tried for ten weeks in 44 pseudo-neurotic patients. Unsuccessfully used tranquillizers were continued and the use of the antiparkinsonian agent dexetimide was allowed if needed. By the end of the study, a considerable improvement was observed for the vast majority of the items of the Wittenborn psychiatric scale. Their socio-professional adaptation showed a similar tendency. Dexetimide was required in four patients who received high doses of pimozide.

Adolescent↗
PubMed1980

Lack of behavioral supersensitivity to d-amphetamine after pimozide withdrawal. A trial with schizophrenic patients.

The dopamine hypothesis of schizophrenia claims that increased dopamine activity underlies psychotic behavior. This hypothesis gets major support from the reported d-amphetamine-induced worsening of psychosis, because amphetamine increases dopamine activity in the brain. Dopamine receptor supersensitivity has been shown to be present in animals during the postneuroleptic period. In this study the postulated relationships between psychotic decompensation as observed after d-amphetamine infusion and the dopamine receptor supersensitivity expected to be present during the neuroleptic withdrawal period were examined. Twenty milligrams of d-amphetamine administered intravenously did not cause a stronger psychotogenic effect in 12 schizophrenic patients. One week after discontinuation of pimozide treatment, the d-amphetamine-induced change as indicated by the Brief Psychiatric Rating Scale (BPRS) paranoid disturbance cluster score, was not significantly different from the response to a similar infusion during the drug-free state. Unexpectedly, the increase in the BPRS mannerisms and posturing item and in the pulse rate response to d-amphetamine were decreased. These results raise questions about the role of dopamine in d-amphetamine effects and suggest postneuroleptic dopamine receptor subsensitivity. They challenge a simple dopamine hypothesis of schizophrenia.

Adolescent↗
PubMed1978

Effect of pimozide on the cytology of the eel pituitary. II. MSH-secreting cells.

Pimozide, a specific blocker of dopaminergic receptors, was injected for 4 or 9 days in freshwater (FW) eels or eels acclimated to sea water (SW) for 10 or 30 days. The daily dose was 100 or 200 microgram/100 g. Melanophore index values increase in FW and in 1 month-SW injected eels. All the treated fish react by a total or subtotal degranulation of the lead-hematoxylin positive cells in the pars intermedia. These cells were previously identified as alpha-MSH-secreting cells. The MSH cell nuclear area is significantly increased, nucleoli are larger and the endoplasmic reticulum more developed. The intensity of the response is similar in FW and SW eels, but it does not increase with the higher dose. The rapid release of pituitary alpha-MSH is also visualized by immunofluorescence and immunoenzymologic techniques. No effect on the second cell type of the pars intermedia (PAS-positive cell) is detected. The amount of neurosecretory material is often reduced in the neurohypophysis. These results suggest that the hypothalamic inhibitory control of MSH release and synthesis is mediated through dopaminergic fibers in the eel, but other factors cannot be ignored in this regulation.

Animals↗
PubMed1979

Intracranial self-stimulation in orbitofrontal cortex and caudate nucleus of rhesus monkey: effects of apomorphine, pimozide, and spiroperidol.

Rhesus monkeys were prepared with stimulating electrodes implanted into the orbitofrontal cortex and head of the caudate nucleus under stereotaxic control. These regions of the brain contain high levels of dopamine, and intracranial self-stimulation was readily elicited from these loci in all animals tested using licking behavior as the operant response. Self-stimulation at both sites was significantly attenuated following peripheral injections of the dopamine receptor blocker spiroperidol (0.02 mg/kg). Similarly, pimozide (0.15 and 0.20 mg/kg) significantly reduced self-stimulation in the orbitofrontal cortex, but the suppression observed at caudate placements did not reach statistical significance. Licking for a reward of blackcurrant juice was unaffected by either drug. Apomorphine (0.2, 0.4 mg/kg) had a differential effect on self-stimulation. This drug significantly attenuated self-stimulation in the orbitofrontal cortex, while the same treatment tended to facilitate self-stimulation in the caudate. Apomorphine did not significantly affect responding for the fruit juice reward. The parallels between the effects of dopamine agonists and antagonists on self-stimulation in the monkey and rat suggest that dopamine influences self-stimulation of some sites in both the primate and the rat.

Animals↗
PubMed1979

The effect of propranolol phentolamine and pimozide on drug-induced anorexia in the mouse.

Pimozide was a potent antagonist of (+)amphetamine, diethylpropion, mazindol and phentermine anorexia in the mouse. Phentolamine and propranolol produced no such antagonism, but either potentiated or had no effect on the drug-induced anorexia. Although the mechanism of action of the four anorectic agents appears to involve dopamine receptor agonist activity, an antagonist or partial agonist effect at noradrenergic receptors may also be involved.

Animals↗
PubMed1984

Opposite action of m-chlorophenylpiperazine on avoidance depression induced by trazodone and pimozide in CD-1 mice.

m-Chlorophenylpiperazine (CPP) given in doses up to 2 mg/kg did not affect conditioned avoidance responses (CAR) of CD-1 mice pre-trained in a shuttle box. It reversed the inhibitory action of trazodone (10 mg/kg) on CAR, but dose-dependently potentiated the inhibitory effect of pimozide (0.2 and 0.5 mg/kg). Apparently, dopaminergic transmission is important for the attenuating effect of CPP on CAR inhibition.

Animals↗
PubMed1980

Changes in blood-brain permeability resulting from D-amphetamine, 6-hydroxydopamine and pimozide measured by a new technique.

A new technique is described for measurement of diffusion across the blood-brain barrier using intraventricularly administered 68Ga-EDTA, and determining loss from the brain with a scintillation camera. Repeated injections via permanent cannulas showed that the diffusion half-time was reduced to 50% of control values after intraventricular d-amphetamine and 6-hydroxydopamine; pimozide had no effect.

Animals↗
PubMed1979

Pimozide and p-chlorophenylalanine blockade in DL-amphetamine and pargyline-treated rats held at two environmental temperatures.

In rats, treated with DL-amphetamine + monoamine oxidase inhibitor, and held at an ambient temperature of 28.5 degrees C, hyperthermia was completely eliminated by treatment with pimozide + p-chlorophenyl-alanine. The same drugs markedly reduced the hypothermic effects in rats treated similarly at 4 degrees C. Results implied that serotoninergic and dopaminergic neurones were involved in the thermoregulatory effects of amphetamine.

Amphetamines↗
PubMed1976

Effects of apomorphine and of pimozide on renin secretion in the anaesthetized dog.

This paper presents the results of a study of the receptors involved in renin hypersecretion induced by dopamine. Apomorphine induces renin hypersecretion without significantly modifying the renal blood flow. This renin hypersecretion is inhibited by haloperidol. However, pimozide, a selective dopaminolytic agent, is incapable of inhibiting the renin hypersecretion induced by dopamine. These results provide supplementary evidence for the existence of renal dopaminergic receptors which would appear to differ from the central dopaminergic receptors.

Animals↗
PubMed1978

Potentiation of morphine hyperthermia in cats by pimozide and fluoxetine hydrochloride.

Administration of morphine sulfate (1--4 mg/kg i.v.) to cats produces changes in body temperature, with hyperthermia appearing with larger doses. Since the central neurotransmitters dopamine and serotonin have been implicated in thermoregulation, studies were done to determine whether morphine's action could be mediated via these transmitters. Temperature responses were measured in freely moving cats by means of rectal thermometer probes. Either pimozide, 0.5 mg/kg i.p., a specific DA receptor blocker, or fluoxetine HCl, 10 mg/kg i.p., a specific inhibitor of 5-HT uptake, was administered 2--3 h prior to morphine injection. Temperatures were monitored for 3.5 h after morphine administration. Both agents were found to enhance the hyperthermic response to morphine with the maximum morphine effect occurring in most cases by 2 h. The results indicate that a balance in the ratio of 5-HT : DA may be involved in cat thermoregulation and that the hyperthermic response in the cat to morphine may be effected by shifting this 5-HT : DA ratio.

Animals↗
PubMed1978

Phencyclidine-induced stereotyped behavior in monkeys: antagonism by pimozide.

The psychotomimetic substance, phencyclidine (PCP), was administered chronically to selected members of a primate social colony. PCP induced stereotyped behavior in all treated monkeys at each of three test doses. Furthermore, there was a significant increase in the amount of stereotypy seen during the second and third weeks of treatment compared to the first week. The dopamine receptor blocking agent pimozide antagonized PCP stereotypy. The results are discussed in terms of dopamine mediation of these responses.

Animals↗
PubMed1983

Effects of pimozide and des Gly10,[D-Ala6]luteinizing hormone-releasing hormone ethylamide on serum gonadotropin concentrations, germinal vesicle migration, and ovulation in female goldfish, Carassius auratus.

In gravid female goldfish held at 10-12 degrees, a single injection of des Gly10,[D-Ala6]luteinizing hormone-releasing hormone ethylamide (LHRH-A), or 2 injections of LHRH-A given 12 hr apart, increased serum gonadotropin (GtH) concentrations, but did not stimulate germinal vesicle migration or ovulation. Injection of a dopamine antagonist, pimozide (PIM), increased serum GtH levels. PIM injected with the second of two LHRH-A injections not only potentiated the LHRH-A-induced increase in serum GtH concentrations but also caused germinal vesicle migration and ovulation. PIM injected with, or in place of, the first of two LHRH-A injections increased the frequency of ovulation in fish injected with LHRH-A. Similarly, PIM injected simultaneously with a single LHRH-A injection also increased the number of ovulating fish. These results are consistent with the idea that dopamine inhibits GtH release in goldfish. The results also suggest that the preovulatory surge of GtH secretion is regulated by both a stimulation by GtH-releasing hormone and release from the dopamine inhibition on GtH secretion.

Animals↗
PubMed1985

Pimozide modulates the luteinizing hormone-releasing hormone effect on gonadotrophin release in the African catfish, Clarias lazera.

In the African catfish the effect of (i) the dopamine antagonist pimozide (PIM), (ii) a luteinizing hormone-releasing hormone analog (LH-RHa), and (iii) a combination of these substances on gonadotrophin (GTH) release and on ovulation was investigated. PIM alone increased plasma GTH levels in juvenile catfish but was ineffective in mature animals. LH-RHa increased plasma GTH levels in both juvenile and mature catfish and within 12 hr after the injection a high rate of ovulation (80%) was observed. PIM potentiated the LH-RHa effect on GTH release and ovulation. It was concluded that dopamine does not effect the GTH release directly, but modulates the effect of endogenous and exogenous gonadotrophin-releasing hormone.

Animals↗
PubMed1988

Effects of [D-Arg6, Trp7, Leu8, Pro9NEt]-luteinizing hormone-releasing hormone (sGnRH-A) and [D-Ala6, Pro9NEt]-luteinizing hormone-releasing hormone (LHRH-A), in combination with pimozide or domperidone, on gonadotropin release and ovulation in the Chinese loach and common carp.

The effects of LHRH-A and sGnRH-A alone and in combination with the dopamine receptor antagonists pimozide (PIM) and domperidone (DOM) on stimulation of gonadotropin (GtH) secretion and ovulation in Chinese loach (Paramisgurnus dabryanus) and common carp (Cyprinus carpio) were studied. When tested in the absence of a dopamine receptor antagonist, sGnRH-A was about 10-fold more potent than LHRH-A in stimulating GtH secretion in loach, whereas these peptides were of similar effectiveness in common carp. Both peptides were effective alone in inducing ovulation in loach, but were ineffective in common carp. PIM and DOM stimulate a small but significant increase in serum GtH, and greatly potentiate the effects of LHRH-A and sGnRH-A on GtH secretion and ovulation in both species. DOM was of equal or somewhat greater potency than PIM in potentiating the action of releasing hormone agonists in loach; however, DOM had markedly greater effectiveness in common carp. sGnRH-A in the presence of DOM was more effective than LHRH-A in stimulating GtH secretion and ovulation in common carp. The present studies suggest that there are marked differences in the relative contribution of GnRH and dopamine in the control of GtH secretion in loach and common carp, and indicate in particular that the more intense dopaminergic inhibitory control of GtH release in common carp modifies the responsiveness of the pituitary to GnRH peptides.

Animals↗
PubMed1987

Lateral hypothalamic stimulation-produced analgesia: inferred refractory period of directly stimulated neurons and resistance to pimozide antagonism.

Electrical stimulation in lateral hypothalamic sites (ESLH) supporting appetitive behavior and reward also diminishes pain and aversion responses that are organized high in the neuraxis. A paired-pulse stimulation technique was used, in two different behavioral paradigms, to infer the absolute refractory periods of LH neurons that mediate this apparent supraspinal analgesia. In both paradigms, recovery from refractoriness--reflected by increased analgesic action--was evident at intrapair intervals of 0.8 msec and greater. This finding suggests that the overlap, if any, between first stage neurons mediating analgesia and appetitive/reward behavior may be restricted to the 'heterogeneous slow population' distinguished by Gratton and Wise. The dopamine antagonist pimozide, at doses known to diminish ESLH-induced feeding and reward (0.25 and 0.5 mg/kg), failed to affect analgesia. Thus, the dopaminergic second stage neurons deemed critical to feeding and reward may not play an important role in analgesia. Finally, ESLH-induced ameliorative action as a case of 'aversion-gating' or a dimension of classical somatosensory analgesia is discussed.

Analgesia↗