Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “METHYSERGIDE”

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 73 records · Page 4Linked to original sources
PubMed1986

Effects of methysergide on the cough reflex.

The present study had two basic purposes: to observe the effect of methysergide on the cough reflex and to investigate the effect of methysergide on the antitussive effect of dextromethorphan. Male and female cats were anesthetized with pentobarbital-Na. Respiration and cough reflex were measured using a pneumotachograph via a cannula inserted into the trachea. The cough reflex was elicited by electrical stimuli to the superior laryngeal nerve. Methysergide (3 mg) injected into the vertebral artery increased the number of coughs and respiratory frequency. Dextromethorphan in a dose of 3 mg inhibited the cough reflex. Methysergide (1 and 3 mg) reduced the antitussive effect of dextromethorphan in a dose-dependent manner, but did not inhibit the excitatory effect on respiratory frequency. These findings might indicate that the central serotonergic system has an inhibitory role on the cough reflex and may be related to the antitussive mechanisms of dextromethorphan.

Animals↗
PubMed1992

Improvement of sexual behavior in aged rats by p-chlorophenylalanine and methysergide.

The effects of methysergide, a serotonin antagonist, and p-chlorophenylalanine (PCPA), a serotonin synthesis blocker on the sexual behavior of intact old male rats at 19-23 months of age and female rats at 17-18 months of age were studied. Female rats with prolonged vaginal cornification and a lordosis quotient (LQ) of less than 50%, and male rats displaying no ejaculation were selected as experimental animals. The receptivity of aged female rats, but not the approach behavior to males nor proceptivity was improved by PCPA or methysergide. The LQ of intact aged female rats in non-exit tests was improved by the i.p. administration of 50 mg/kg B.W. of PCPA 2 to 4 hours prior to the sexual behavior test or 3 mg/kg B.W. of methysergide 4 hours prior to the test. Total mount frequency and mount latency of intact aged male rats were improved by the administration of methysergide (3 mg/kg B.W.), while total mount frequency and intromission latency were improved by the administration of PCPA (20 mg/kg B.W. for 4 days). The present results together with the finding from our previous study suggest that the increase of serotonin (5-HT) activity per se plays an important role in the decline of receptivity of aged female rats and the copulatory activity of aged male rats.

Aging↗
PubMed1989

Methysergide-induced nipple attachment depends on suckling experience in juvenile rats.

These studies were designed to investigate the links between pharmacological and behavioral procedures that facilitate suckling in weanling rats by assessing the effects of methysergide on nipple attachment behavior following experiential manipulations known to either promote or attenuate suckling. In the first experiment, methysergide failed to stimulate suckling in 25-day-old rats separated from their dam on Day 20, although it facilitated suckling in rats kept with the dam until either Day 24 or Day 25. In the second experiment, methysergide did not facilitate suckling in 35-day-old rats separated on Day 25, although rats separated on Day 30 or 34 were induced to suckle. In the third experiment, rats were housed with preweanling litters until Day 35 and then separated, housed with 25-day-old litters, or housed with preweanling litters for another 10 days. Rats in a fourth group remained with their dams until Day 35 and were then separated for 10 days. When tested at Day 45, nipple attachment was facilitated by methysergide only in the three groups that had received extended suckling experience. These results demonstrate that serotonergic inhibitory mechanisms modulate nipple attachment only when suckling experience is recent or extensive.

Animals↗
PubMed1986

Methysergide-induced lower extremity arterial insufficiency.

Lower extremity arterial insufficiency, a relatively common complication of ergotamine ingestion, is a rare complication of methysergide therapy for migraine headaches. Methysergide causes one of two typical angiographic patterns: intra-abdominal extrinsic compression of the aorto-iliac vessels in patients with retroperitoneal fibrosis, or marked diffuse bilateral spasm of the superficial femoral arteries in those without retroperitoneal fibrosis. We report a patient with methysergide-induced bilateral lower extremity arterial spasm and review the relevant literature. When one of the above arteriographic patterns is recognized, methysergide ingestion should be considered as a possible etiology.

Female↗
PubMed1981

Dual actions of lysergic acid diethylamide tartrate (LSD), 2-bromo-D-lysergic acid diethylamide bitartrate (BOL) and methysergide on dorsal root potentials evoked by stimulation of raphe nuclei.

A variety of drugs reported to antagonize serotonin were found to affect spinal cord potentials evoked by electrical stimulation of the caudal raphe nuclei of the cat. These brain stem-evoked dorsal root potentials (DRPs) consisted of a short latency depolarization (DRP-1), which was evoked by stimulation of a wide variety of sites in the medial brain stem and a long latency potential (DRP-2), which was elicited only when stimuli were applied near the raphe. The ability of serotonergic antagonists to increase or decrease these DRPs was dependent on the dose of the drug administered. High doses of lysergic acid diethylamide tartrate (LSD), 2-bromo-D-lysergic acid diethylamide bitartrate (BOL), methysergide and cinanserin each produced an immediate inhibition of DRP-2 and a simultaneous enhancement of DRP-1, both of which recovered by approximately 30 min. Each of the drugs produced a dose-related inhibition of DRP-2 at high doses, with LSD being the most potent and cinanserin the least potent. In contrast, low doses of LSD, BOL and methysergide elicited little or no immediate change in either DRP-2 or DRP-1, but produced an enhancement of DRP-2 which developed slowly over a period of 60 to 90 min. This increase in DRP-2 was most dramatic after administration of LSD and was not accompanied by changes in DRP-1. The inhibition of DRP-2 by high doses of LSD, BOL, methysergide and cinanserin may result primarily from inhibition of postsynaptic serotonergic receptors located on the primary afferent terminals. The increase in DRP-2 produced by low doses of LSD, BOL and methysergide is postulated to result from an interaction with receptors distinct from those which produced the inhibition of DRP-2 at higher doses.

Animals↗
PubMed1999

The association of the combination of sumatriptan and methysergide in myocardial infarction in a premenopausal woman.

Acute myocardial infarction occurred in a 43 year-old premenopausal woman with controlled hypertension and no known coronary artery disease following the use of the antimigraine medications sumatriptan succinate injectable form and methysergide maleate. The use of sumatriptan is contraindicated within 24 hours of using ergotamine or ergotamine-type medications such as methysergide. This contraindication is based on the theoretical possibility of prolonged vasospasm with the combined use. Methysergide is primarily a serotonin type 2 (5-HT2) antagonist, although it does act as a partial agonist at 5-HT1 receptors. It is believed that a major component of coronary artery vasospasm is possibly due to 5-HT supersensitivity mediated by 5-HT1Dbeta receptor activation. Drugs that selectively stimulate the 5-HT(D) receptors, such as sumatriptan, are potentially hazardous in people with underlying coronary artery disease, and agents with additional agonistic properties at these receptors may potentiate this effect. Physicians should be warned to inquire about prior 24-hour medication use before prescribing antimigraine medication.

Adult↗
PubMedDate not supplied

Prophylaxis of migraine attacks with a calcium-channel blocker: flunarizine versus methysergide.

In this study, flunarizine, a selective calcium-channel blocker, was employed in the prophylactic treatment of headache and was compared with methysergide in terms of efficacy. The trial was conducted with 104 patients (53 treated with flunarizine and 51 treated with methysergide) and lasted six months--one month of pretreatment and five months of therapy. Patients in both groups experienced a highly significant reduction in the number and duration of migraine attacks. Unlike those in the methysergide group, patients treated with flunarizine achieved a significant reduction in the intensity of attacks with very negligible side effects.

Adult↗
PubMed1988

Increased food intake in satiated rats induced by the 5-HT antagonists methysergide, metergoline and ritanserin.

Two series of experiments examined whether 5-hydroxytryptamine (5-HT) antagonists induce feeding in rats. In the first series of experiments separate groups of rats were injected with various doses of methysergide, cyproheptadine, metergoline or ritanserin prior to a 2 h period of access to a wet mash diet which induced vigorous feeding under control conditions. None of the antagonists increased food intake in this paradigm. Rather, at certain doses, methysergide, cyproheptadine and ritanserin induced slight decreases in food intake. Since 5-HT may be involved in controlling satiety, it may be that a more appropriate test of the efficacy of these compounds involves administering them to maximally satiated rats. Consequently, the effects of these drugs were investigated in groups of rats which had fed to satiety immediately prior to drug treatment. In this paradigm methysergide, metergoline and ritanserin, but not cyproheptadine, induced definite increases in food intake. It is suggested that this effect occurs via a dissipation of satiety signals, and that these results further support the hypothesis that 5-HT is involved in controlling satiety. The possibility that these antagonists act on peripheral 5-HT systems is discussed.

Animals↗
PubMed1980

Effect of two antiserotoninergic drugs, methysergide and metergoline, on gastric acid secretion and gastrin release in healthy man.

The effects of acute oral administration of the antiserotoninergic drugs methysergide (3 mg) and metergoline (4 mg) on basal, submaximal (0.6 micrograms/kg i. m.) and maximal (6 micrograms/kg) pentagastrin-stimulated gastric acid secretion, as well as on basal and food-induced gastrin release, have been evaluated in healthy volunteers. Methysergide significantly increased basal and submaximal pentagastrin-stimulated gastric acid secretion, and metergoline significantly inhibited gastric acidity in all experiments. Basal and stimulated serum gastrin concentrations were not modified by either drug. The effect of methysergide on gastric acid secretion was opposed to that of serotonin and was probably dependent on its antiserotoninergic action, but the decrease in gastric acidity caused by metergoline is not easily explained. Although the effect is similar to that of a dopamine infusion, it does not depend on dopamine infusion, it does not depend on dopamine receptor stimulation, since it was not influenced by pretreatment with metoclopramide. It is suggested that it might be due to the weak anticholinergic and/or antihistaminic properties of metergoline.

Adult↗
PubMed1986

Chronic beta-adrenergic stimulation increases in mice the sensitivity to methysergide and the number of cerebral high affinity serotonin binding sites (5-HT-1).

Reserpine administration in mice causes, among other effects an akinesia which can be reversed by the serotonin agonist-antagonist methysergide. The effect of methysergide is potentiated by clenbuterol, a beta-adrenergic agonist, which itself causes hypomotility. Potentiation is weak after a single injection of clenbuterol, but becomes much stronger after repeated administration for 12 days. This treatment also causes a 50% increase in the number of high affinity 5-HT-1 binding sites in the brain. This increase would explain the increased potency of methysergide against reserpine-induced akinesia. These results show that: a beta-adrenergic drug, clenbuterol modulates the serotoninergic system; this modulation takes its importance after chronic treatment only; this interrelation may be important in depressive illness since it is observed on a test used in the screening of antidepressant drugs.

Animals↗
PubMed1984

Inflammatory pleuropulmonary fibrosis in essential fatty acid deficient rats and the lack of response to methysergide.

In view of the association between essential fatty acid (EFA) deficiency and human cystic fibrosis, we have investigated the possible occurrence of pulmonary disease in rats fed an EFA deficient (EFAD) diet for 40 weeks. In contrast to a few slight spontaneous lesions consisting of pleural membrane hyperplasia, which were found in the lungs of control rats, a much greater incidence of fibrotic lesions was observed in the lungs of EFAD rats. These pleuropulmonary fibroses extended from the hyperplastic pleural membrane into the alveoli and were characterized by collagen deposition and marked macrophage infiltration to the extent that, in some cases, the alveolar septa were completely obstructed by inflammatory exudate. These findings lend indirect support to the contention that EFA deficiency plays a role in the aetiology of cystic fibrosis, at least with regard to pulmonary lesions. Administration of methysergide (10 mg/kg/day, p.o.) for a total of 11 weeks, did not alter the incidence of fibrosis in the lungs of EFAD rats, despite the finding that a man who had developed pleuropulmonary fibrosis as a result of chronic methysergide treatment exhibited a relative serum EFA deficiency. While a relative EFA deficiency may be a predisposing factor for the induction of fibrosis by chronic methysergide treatment, our data are not sufficient to make a decision upon this hypothesis.

Adult↗
PubMed1992

Effects of combined methysergide and mecamylamine/scopolamine treatment on spatial navigation.

In the present study, we investigated the effects of a 5-HT2 receptor antagonist, methysergide (2.5, 7.5 and 20 mg/kg), on spatial learning in saline, mecamylamine (10 mg/kg) and scopolamine (0.8 mg/kg) treated rats. Methysergide had no effect on water-maze (WM) spatial learning in rats subjected to saline or mecamylamine pretreatments. However, scopolamine-induced WM learning deficit was augmented by methysergide at doses of 7.5 and 20 mg/kg. These results further suggest (A) that cholinergic and serotonergic systems may interact in the regulation of spatial learning, and (B) that the cholinergic component of this interaction with serotonin2 receptors is mediated by muscarinic receptors, but not by nicotinic receptors.

Animals↗
PubMed1978

Effects of methysergide, pizotifen and ergotamine in the monkey cranial circulation.

Internal and external carotid vascular resistances were measured, in anaesthetized monkeys, to asses the direct cranial vascular effects of i.v. methysergide, pizotifen and ergotamine, and their effects on the cranial vascular responses to the constrictors 5-hydroxytryptamine and noradrenaline and the dilators histamine, prostaglandin E1 and bradykinin. Methysergide reduced responses to 5-HT, and tended to potentiate the external carotid responses to noradrenaline. Pizotifen blocked responses to histamine; it tended to reduce internal carotid responses to 5-HT, but it potentiated external carotid 5-HT responses. Ergotamine reduced responses to 5-HT and noradrenaline, but this was probably related to its cranial vasoconstrictor effects, especially in the external carotid circulation. Methysergide induced weak transient cranial vasoconstriction and pizotifen had no direct effects. These findings may be relevant to the therapeutic actions of these drugs in migraine, since the doses used approximated to those used clinically.

Animals↗
PubMed1981

Effects of methysergide on some cardiovascular responses in the anaesthetized rabbit.

Methysergide (0.1-5 mg/kg i.v.) caused dose-dependent reductions in the resting heart rate of anaesthetized rabbits. Resting mean arterial blood pressure was reduced only after the maximum dose. Methysergide 5 mg/kg significantly enhanced the pressor responses to i.v. phenylephrine and enhanced the accompanying bradycardia disproportionately. There was no evidence for a central increase in baroreflex gain, so an action of methysergide on baroreceptor sensory endings is suggested as a possible explanation.

Anesthesia↗
PubMed1986

Regional serotonin receptor studies: chronic methysergide treatment induces a selective and dose-dependent decrease in serotonin-2 receptors in mouse cerebral cortex.

Compared with the well described supersensitization responses of dopaminergic and beta-adrenergic receptors to pharmacologic antagonists and denervation, the regulation of serotonin-1 (S-1) and serotonin-2 (S-2) receptors is poorly understood. In an effort to modulate S-1 and S-2 receptors in mouse brain, male C57BL/6J mice were treated chronically with methysergide, a serotonin antagonist with nanomolar affinity for both S-1 and S-2 receptors. Methysergide treatment had no influence on the affinity or density of S-1 receptors as measured by binding of (3H)-5-HT in cerebral cortex, hippocampus or hypothalamus. In contrast, the S-2 receptor specific binding of (3H)-spiperone in the cerebral cortex decreased in a dose dependent fashion, a direction of change opposite to that usually seen in catecholamine pathways chronically exposed to antagonists. The effect was selective for the S-2 serotonergic receptor since the D-2 dopaminergic receptor specific binding of (3H)-spiperone in the caudate nucleus was unaffected by drug treatment. These results suggest that either serotonin receptors respond atypically to chronic receptor blockade by antagonist or that in vivo, methysergide may have additional pre-synaptic effects on serotonin uptake or release.

Animals↗
PubMed1993

Further evidence that prolactin secretion in adult female rats is differently modified after neonatal estrogenization or androgenization: responses to methysergide, quipazine, and pizotifen.

The role of the serotoninergic system in the control of prolactin secretion was investigated in adult female rats treated on the first day of life with estradiol benzoate (EB) (100 micrograms), testosterone propionate (TP) (25 or 100 micrograms), or olive oil. Blood of rats was obtained through a chronic intraatrial cannula at 0, 30, 60, 90, and 120 min after the IP administration of the serotoninergic blockers methysergide (0.75, 2.5, and 7.5 mg/kg) or pizotifen (2 mg/kg), the agonist quipazine (3 or 30 mg/kg), or saline. We have found that 1) the anovulatory syndrome induced by EB or 100 micrograms injection of TP was associated with hyperprolactinaemia, whereas normal prolactin concentrations in plasma were observed in females injected with 25 micrograms of TP; 2) methysergide administration increased plasma prolactin concentrations in control and androgenized females but not in the estrogenized ones. This different response may be related to the antidopaminergic action of methysergide, because both estrogenized and androgenized females responded similarly after pizotifen injection; 3) after quipazine injection, an initial stimulation was observed in females injected with estradiol or 100 micrograms of TP, but not in other groups, whereas a delayed inhibition occurred in androgenized females. These results suggest that the effects of estrogenization and androgenization on both the dopaminergic and serotoninergic control of prolactin secretion are qualitatively different.

Animals↗
PubMed1978

Biphasic effects of the antiserotonergic methysergide on lordosis in rats.

As also reported by other workers, the antiserotonergic drug methysergide was found to facilitate lordotic responding in estrogen primed, ovariectomized rats. A second dose of methysergide 24 hr after the first, however, failed to produce any increment in responding. Animals received daily estrogen injections in order to maintain a relatively constant level of priming. After several days of methysergide, a progesterone injection facilitated lordosis to the same degree as in controls receiving only saline and estrogen. When a second injection of progesterone was given 24 hr later, however, the animals failed to respond. In contrast, saline controls with this estrogen paradigm responded equally well to both progesterone injections. These results are discussed in terms of their bearing on possible serotonergic and non-serotonergic mechanisms by which progesterone may control lordosis.

Animals↗
PubMed1985

Effects of quipazine and methysergide on play in juvenile rats.

Social play of juvenile rats was analyzed following administration of either the serotonin receptor agonist quipazine (1, 2.5, 5 and 10 mg/kg) or the antagonist methysergide at the same doses. Quipazine reduced pinning at all doses, while methysergide did so at only the highest two. An interaction study using the lowest doses of the agents used above, indicated that methysergide could reverse quipazine induced reductions of play. Thus, the quipazine effect was probably mediated through a serotonin receptor; however, the role of serotonin in play appears to be a general modulatory one rather than a specific influence on play.

Animals↗