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At least 145 records · Page 8Linked to original sources
PubMed1975

Effect of methysergide, a blocker of serotonin receptors, on plasma prolactin levels in lactating and ovariectomized rats.

The effect of methysergide (MES, 2.5 mg/100 g body wt), a serotonin antagonist, on prolactin release has been studied in lactating and ovariectomized rats. MES caused significant increases in prolactin release in both animals. Studies in ovariectomized, hypophysectomized rats indicate that this effect is not due to a decrease in the peripheral metabolism of prolactin. In vitro incubations of anterior pituitary fragments with MES failed to demonstrate any increase in prolactin release, suggesting that MES does not act directly on the anterior pituitary. Parachlorophenylalanine (PCPA; 32 mg/100 g body wt) decreased brain serotonin levels in ovariectomized rats 5, 24, and 70 h after its administration, yet did not alter plasma prolactin levels. L-tryptophan (6.3 mg/100 g body wt) given 1 and 1 1/2 h prior to sacrifice increased brain serotonin levels, yet did not affect plasma prolactin levels. Neither PCPA nor L-tryptophan altered MES-induced prolactin release. In lactating rats, suckling caused marked increases in plasma prolactin levels, an effect completely abolished by the administration of MES to the mother rats 3 1/4 h prior to suckling. However, MES-induced prolactin release was not altered by prior treatment with MES, either in lactating or ovariectomized rats. Others have shown that suckling releases prolactin through an excitatory serotonergic mechanism. Therefore, the failure of suckling to release prolactin in MES-pretreated rats suggests that MES can block brain serotonin receptors. However, the ability of methysergide to release prolactin in rats with serotonin receptors presumably blocked, suggests that the serotonin receptor-blocking and the prolactin-releasing actions of MES are not related.

Animals↗
PubMed1979

The effect of methysergide, pimozide, and sodium valproate on the diazepam-stimulated growth hormone secretion in man.

Diazepam-induced GH secretion was tested on 28 male volunteers before and after a 3-day treatment with methysergide, pimozide, or sodium valproate. Serum GH, diazepam, and blood glucose levels were determined. Without prior medication, the mean serum GH level increased 336% 1 h after diazepam administration. Treatment with the serotonin antagonist, methysergide, had no effect on the diazepam-stimulated GH secretion, whereas pimozide, the selective dopamine receptor-blocking agent, reduced the GH response to diazepam by 50% (P less than 0.05). Sodium valproate, a gamma-aminobutyric acid transaminase inhibitor, also inhibited diazepam-induced GH secretion; stimulated GH levels were 51% at 30 min (P less than 0.025), 39% at 60 min (P less than 0.025), and 46% at 90 min (P less than 0.025) relative to the stimulated levels without medication. No difference was found in blood glucose or serum diazepam levels after the drug treatments relative to the values obtained under basal conditions. It is suggested that diazepam-induced GH secretion is at least partly mediated via dopaminergic mechanisms. Serotonin does not seem to be involved. It is further proposed that gamma-aminobutyric acid plays an inhibitory role in GH secretion.

Adult↗
PubMed1981

Progressive supranuclear palsy: functional analysis of the response to methysergide and antiparkinsonian agents.

Twelve patients with progressive supranuclear palsy were treated with methysergide; the response was monitored with videotaped examination, electrooculography, and psychometric assessment. Used alone and with antiparkinsonian agents, methysergide improved the quality of life in eight patients for 6 months to 2 years. Benefits were especially dramatic in four patients with severe dysphagia. The disorder of visually guided behavior included abnormal orienting responses, visuosocial expression and regard, and visual search. Mesencephalic visuomotor centers appear to be important not only in control of ocular motility but also in the elaboration of visually guided behavior and the orienting of spatial attention.

Aged↗
PubMed1995

Effect of antihistamines, disodium cromoglycate (DSCG) or methysergide on post-irradiation cerebral blood flow and mean systemic arterial blood pressure in primates after 25 Gy, whole-body, gamma irradiation.

Exposure to ionizing radiation causes hypotension, cerebral ischemia and release of histamine (HA) and serotonin (5-HT). To investigate the relationship among these responses, rhesus monkeys (Macaca mulatta) received physiological saline (i.v.), disodium cromoglycate (DSCG), antihistamines (AH, mepyramine and cimetidine), or methysergide (METH), then were given 25 Gy whole-body irradiation. Monkeys receiving DSCG, AH or METH had higher post-irradiation mean arterial blood pressure (MBP) than saline-treated controls. Compared to levels in controls, post-irradiation hippocampal blood flow (rCBF) levels were higher in monkeys receiving DSCG, AH or METH. Treatment with the 5-HT2 receptor antagonist methysergide was the most effective in maintaining both rCBF and MBP after irradiation. Results support the hypothesis that the irradiation-induced cerebral ischemia and, to some extent, the hypotension is mediated by serotonin through 5-HT2 receptor sites.

Animals↗
PubMed1997

Methysergide-induced retroperitoneal fibrosis: successful outcome and two new laboratory features.

A 25-year-old woman sought medical attention because of iliocaval manifestations of retroperitoneal fibrosis while she was taking methysergide. Laboratory studies yielded substantially increased serum procollagen III levels and anticardiolipin antibodies accompanied with anti-beta(2) glycoprotein I, findings not previously described with this disorder. Clinical and laboratory manifestations resolved after cessation of methysergide therapy.

Adult↗
PubMed1975

The involvement of methysergide-sensitive receptors and prostaglandins in the hyperthermia evoked by 5-HT in the cat.

In the unanesthetized cat, an injection of 0.01 or 0.03 M 5-hydroxytryptamine into the rostral hypothalamus produced an immediate, short-lasting increase or decrease in body temperature. A delayed and long-lasting hyperthermia often followed the initial response. When indomethacin, 10 mg/kg, was administered intraperitoneally 3 hours prior to an injection of 5-hydroxytryptamine at sites which produced an initial increase in body temperature, the secondary hyperthermia was reduced or abolished but the immediate response remained undiminished. Pretreatment with methysergide, 2 mg/kg i.p., attenuated or abolished the initial temperature increase but did not reduce the delayed hyperthermia. The results suggest that the initial rise in body temperature produced by 5-hydroxytryptamine is mediated by activation of methysergide-sensitive 5-HT receptors and that the response is independent of prostaglandin release. The secondary hyperthermia, on the other hand, is apparently mediated by a sustained release of prostaglandins.

Analysis of Variance↗
PubMed1975

The effect of ergotamine and methysergide on serotonin metabolism in the rat brain.

Ergotamine tartrate and methysergide maleate each significantly altered serotonin (5-HT) metabolism in the rat brain. Whole brain levels of 5-HT were markedly reduced in a dose-related manner, with peak activity observed 30 minutes after I.P. administration and persisting through four hours after dosing. In addition, turnover rate of 5-HT was significantly increased. Pentylenetetrazol (PTZ)-induced convulsions were not inhibited by either ergotamine or methysergide but each drug interacted with PTZ to induce lethality, which is suggestive evidence of central 5-HT antagonist activity. Moreover, regional distribution of 5-HT in the rat brain was altered by these drugs in such a way to suggest that neihter was a "universally acting" central 5-HT antagonist.

Animals↗
PubMed1977

The effect of methysergide and other receptor antagonists on fenfluramine-induced glucose uptake into the isolated rat hemidiaphragm.

Fenfluramine in therapeutic concentrations causes a significant and dose related increase in glucose uptake into isolated rat and human skeletal muscle in the presence of insulin. Using fenfluramine, 100 ng/ml, on the rat hemidiaphragm preparation the effects of the following receptor blocking drugs in concentrations up to 250 ng/ml were investigated on this phenomenon: atropine, haloperidol, mepyramine, methysergide, propranolol and thymoxamine. Only methysergide, the 5-HT antagonist, reduced the action of fenfluramine in relatively low concentrations of the drug which were dose related (10 ng/ml causing approximately 40% inhibition). This suggests that the peripheral as well as the central actions of fenfluramine are mediated through 5-HT receptors.

Animals↗
PubMedDate not supplied

[Prophylactic treatment of episodic cluster headaches with methysergide and prednisone].

In two consecutive series of 25 cases each suffering from episodic cluster headache, one of the clusters was treated prophylactically in the first series with methysergide and in the other with prednisone. The duration of the clusters under treatment was similar in both series. The results of our study suggest that neither the methysergide nor the prednisone were able to shorten the duration of clusters.

Adolescent↗
PubMed1981

Effects of methysergide or phenoxybenzamine on the renal and cardiovascular responses to endotoxin in rats.

Renal and cardiovascular responses to an intravenous infusion of endotoxin (2.5 mg/kg/hr for four hours) were studied in unanesthetized rats. Cardiac output was reduced while total body and renal vascular resistance increased. Mean systemic blood pressure was only slightly reduced. The renal excretion of sodium, potassium, and water were reduced with no significant effect on urine concentration. Glomerular filtration rate, renal plasma flow, and filtration fraction were also reduced. alpha-Adrenergic blockade with phenoxybenzamine did not prevent any of the above changes, but a 5-HT blocking agent, methysergide, greatly reduced the effect of endotoxin on total peripheral resistance and blocked the effect of endotoxin on renal vascular resistance and renal blood flow. In rats treated with phenoxybenzamine or methysergide, endotoxin caused a large fall in the filtration fraction and extreme reduction in the rate of sodium excretion. These changes possibly resulted from decreases in the glomerular ultrafiltration coefficient or in capillary hydrostatic pressure.

Animals↗
PubMedDate not supplied

[Inhibition of prolactin release by methysergide and bromocriptine in hyperprolactinemic subjects: comparative dynamic studies (author's transl)].

Reduction of hyperprolactinemia by Methysergide (4.4 mg p.o.) and Bromocriptine (2.5 ng p.o.) was studied in 20 patients (7 subjects with pituitary macroadenoma and 13 hyperprolactinemic patients with normal sella turcica). No difference was observed between the effects of the two drugs 4 hours after their administration, with and without respect of the aetiologies of hyperprolactinemia. However the serum prolactin levels were significantly lower 6 hours (n = 11 p = 0,01) and 12 hours (n = 10 p less than 0,01) after Bromocriptine than after methysergide. The difference observed between the two drugs seems to be inherent to their different half-lives.

Adenoma↗
PubMed1977

Methysergide therapy causing vascular insufficiency of the upper limb.

A 41-year-old woman, who was receiving methysergide maleate for the treatment of severe headaches, had occlusion of the left brachial artery, confirmed by arteriography. The occlusion was believed to result from the use of methysergide and the drug was therefore withdrawn. Within 4 days the distal pulses were normal, as confirmed by arteriography, and she was asymptomatic.

Adult↗
PubMed1996

Effect of graded doses of methysergide on basal and pentagastrin stimulated gastric secretion in anaesthetised rats.

The effect of continuous infusion (iv) of graded doses of methysergide (0.1-50 microgram(s)/kg/hr) was studied on basal and pentagastrin (5 microgram(s)/kg/hr) stimulated gastric acid secretion in anaesthetised rats by the slow, continuous stomach perfusion method. Both basal and pentagastrin stimulated acid secretion indicated a biphasic response. Methysergide induced stimulation at a lower dose of 1 microgram(s)/kg/hr and inhibition at higher doses of 20-50 microgram(s)/kg/hr. The stimulatory effect may be due to postsynaptic receptor blockade while the inhibitory effect at higher dose may be due to blockade of presynaptic 5-HT autoreceptors, or due to a direct inhibitory effect of unknown basis.

Anesthetics↗
PubMed1986

Effects of methysergide, bromocriptine and naloxone on prolactin, growth hormone and TSH release induced by D-Met2,Pro5-enkephalinamide in man.

D-Met2,Pro5-enkephalinamide (EA) 10 mg, given SC, induced a dramatic rise in serum prolactin (PRL) and growth hormone (GH) levels in healthy male volunteers. The TSH content was also moderately elevated. Naloxone 0.8 mg administered IV abolished these effects. Bromocriptine 2.5 mg given per os also antagonized EA-induced PRL and TSH release but potentiated the GH surge. Methysergide 2.0 mg administered orally partially reversed EA-elicited PRL release, further augmented GH liberation and did not modify TSH output. The data indicate that inhibition of the dopaminergic tone and/or activation of certain serotonergic mechanisms play an important role in the EA-induced release of PRL and TSH. However, primarily other neurotransmitters might mediate the GH liberation elicited by this opioid peptide.

Adult↗
PubMed1986

Influence of p-chloroamphetamine and methysergide on the escape deficits provoked by inescapable shock.

The effects of serotonergic manipulations on the escape interference engendered by exposure to inescapable shock were assessed. Consistent with the view that the behavioral interference was related to reductions of serotonin (5-HT), treatment with the 5-HT receptor blocker methysergide mimicked the effects of inescapable shock in that it increased escape latencies. Conversely, acute treatment with a moderate dose of the 5-HT releasing agent p-chloroamphetamine (PCA) effectively antagonized the escape interference ordinarily provoked by inescapable shock. The effects of PCA were behaviorally distinguishable from the previously observed effects of catecholamine stimulants. Whereas catecholamine stimulants applied prior to either inescapable shock or escape testing eliminated the interference, PCA antagonized the behavioral disruption only if it was administered before testing. It is suggested that catecholamine alterations may be fundamental in the provocation of the interference, whereas 5-HT variations may contribute to the expression of the behavioral disturbance.

Amphetamines↗
PubMed1984

Methysergide and metergoline reduce morphine analgesia with no effect on the development of tolerance in rats.

A single subcutaneous injection of 5 mg/kg metergoline or 10 mg/kg methysergide, two serotonin antagonists, or 1 mg/kg naloxone, significantly reduced the effect of a subcutaneous dose of 3 mg/kg morphine in the tail immersion test in rats. The same drugs and doses were administered concurrently with 10 mg/kg morphine twice daily for 3 days and nociceptive responses were measured 96 h later. Tolerance to the effect of 3 mg/kg morphine was comparable in animals which had received vehicle + morphine or serotonin antagonists + morphine, whereas naloxone completely prevented the development of tolerance. The results argue against a role of serotonin in the development of tolerance to the antinociceptive effect of morphine and suggest it may be possible to dissociate morphine analgesia from tolerance development, at least in the conditions used in the present study.

Analgesia↗
PubMed1980

Redistribution of cardiac output during localized granulomatous inflammation and the effect of methysergide in anesthetized rats.

The distribution of cardiac output (CO) to different organs and tissues was determined by the radioactive microsphere technique in anesthetized rats 3, 5, 7, and 10 days after subcutaneous implantation of carrageenan-impregnated sponges to induce granulomatous inflammation. Distribution of CO to organs which usually respond to stress (heart, spleen, adrenals) was increased during the acute-subacute inflammatory response, at the expense of the distribution to the head, brain, abdominal muscle, and hind legs. Later decreases were seen in distribution of CO to the kidneys, tail, forelegs, and urogenitals. Vascular-related skin temperature (measured by thermography) and distribution of CO to the back skin generally showed a decrease, particularly to the skin covering the granuloma. This latter decrease was reversed by systemic treatment with methysergide (40 mg/kg) which also increased distribution of CO to the head and decreased that to the liver. Most of the effects observed can be attributed to the extra burden on the circulation presented by the highly vascularized granuloma tissue and/or to the release of 5-hydroxytryptamine, but may differ from changes in conscious rats.

Anesthesia↗
PubMed1977

Intensification of amphetamine-induced excitation by methysergide, a serotonergic receptor blocker.

Methysergide, a serotonergic receptor blocker, was studied to determine its effects against d-amphetamine-induced excitation as measured by convulsions elicited by handling in mice. Significant intensification (p less than 0.01) of the action of d-amphetamine was observed in mice. These results indicate that reduction in serotonergic activity in the central nervous system enhances excitation induced by d-amphetamine.

Animals↗