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At least 127 records · Page 7Linked to original sources

PubMed1986

Effect of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--I. Growth hormone.

In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker: methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). DMI-induced GH stimulation was not significantly different after DMI i.v. alone (n = 12) than after three days' pretreatment with 12 mg methysergide p.o. in another group of subjects (n = 12). Following combined administration of DMI and propranolol (15 mg i.v.), GH secretion was significantly increased by 25 mg DMI (p less than 0.05) and 50 mg DMI (incomplete block design, n = 18). GH secretion was significantly lower (p less than 0.01) after DMI in combination with 60 mg phentolamine i.v. compared to that after administration of DMI alone in the same group (n = 12). Following 10 mg yohimbine i.v. in combination with DMI (n = 6), the DMI-induced GH increase was also significantly less (p less than 0.05) than that after DMI alone. The DMI-induced GH increase following DMI plus 1 mg prazosin p.o. (n = 12) was comparable to that after DMI alone. The results indicate that the GH-stimulating effect of DMI is primarily related to the ability of DMI to inhibit noradrenaline (NA) reuptake. Should serotonergic receptors be involved in the DMI-induced GH secretion at all, they transmit a positive stimulus. The alpha-1 receptors are most likely not (or not essentially) involved, whereas alpha-2 receptors affect the DMI-induced secretion positively, and beta receptors have an inhibitory effect.

Adolescent↗

PubMed1986

Effects of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--III. Hypothalamo-pituitary-adrenocortical axis.

In this report the effects of various receptor blockers on the desimipramine (DMI)-induced cortisol (ACTH) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker, i.e. methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). In addition, the effect of prazosin on DMI-induced ACTH stimulation was examined. DMI-induced cortisol stimulation was not significantly different after DMI alone (n = 12) from that after three days pretreatment with methysergide (12 mg p.o.) in another group of subjects (n = 12). Neither the combination of DMI plus propranolol (15 mg i.v. n = 18, incomplete block design) nor that of DMI plus phentolamine (60 mg i.v. n = 12) had a significant influence on DMI-induced cortisol secretion. Following combined administration with yohimbine (10 mg i.v.), cortisol secretion was higher compared to that after DMI alone in the same group (n = 6). DMI-induced cortisol secretion was significantly lower (p less than 0.01) following combined administration with prazosin (1 mg p.o. n = 12), as was DMI-induced ACTH secretion (p less than 0.05) in these subjects. The findings of these trials, especially those of the prazosin trial, indicate that DMI-induced stimulation of cortisol and ACTH secretion is attributable to the noradrenaline (NA) reuptake inhibiting effect of DMI, and that the stimulus is transmitted with the aid of noradrenergic alpha-1 receptors. Alpha-2 receptors possibly exert a negative influence on this effect.

Blood Glucose↗

PubMed1999

Combined action of thioperamide plus scopolamine, diphenhydramine, or methysergide on memory in mice.

The aim of the present experiments was to test the role played by the interaction of the selective H3 receptor antagonist, thioperamide, with the cholinergic, histaminergic, and serotonergic systems in modifying memory. The behavioral tests used (open-field and passive-avoidance repetition) were selected on the basis of the action displayed by thioperamide in these behavioral situations. Posttrial administration of thioperamide (5 mg/kg) resulted in an improvement in memory consolidation, as tested in the repetition of the open-field test, but repeated posttrial administration of thioperamide (2 or 5 mg/kg) had no effect in the repetition of passive avoidance test. Scopolamine (2 mg/kg) caused a deterioration in the memory processes in both tests: this effect was blocked by 2 mg/kg of thioperamide, which was itself ineffective in the test. These results may suggest that both the improvement in memory due to thioperamide and its antagonism of the amnestic effects of scopolamine are determined by activation of central cholinergic systems, due to thioperamide inhibition of H3 heteroreceptors. Diphenhydramine (2 or 10 mg/kg) was itself ineffective in the tests, but counteracted the memory improvement caused by thioperamide in the repetition of the open-field test. The effect of diphenhydramine is discussed in terms of interactions between histaminergic and cholinergic systems. Methysergide counteracted the effect of thioperamide in the open-field test only at a high dosage (50 mg/kg). The possible implication of serotonergic systems on the effects of the methysergide-thioperamide interaction in the memory process is discussed.

Animals↗

PubMed1991

[Pleural fibrosis as a side effect of years-long methysergide therapy].

A 58-year-old man was admitted to hospital because of exertional dyspnoea and a cardiac murmur not previously heard. For one year he was known to have left-sided fibrinous pleuritis. For 5 years he had been taking methysergide for cluster headaches. From 1950-1980 he had worked with asbestos-containing insulating material. Erythrocyte sedimentation rate was greatly increased to 117/136 mm and there was an hypochromic anaemia (Hb 10.4 g/dl). The cholestasis enzymes were elevated (gamma-GT 88 U/l; alkaline phosphatase 511 U/l). Computed tomography of the thorax demonstrated left-sided pleural thickening of up to 3 cm. Endocarditis was excluded (sterile blood culture; normal echocardiogram). There was no evidence of an infectious, immunological or malignant cause for the pleural fibrosis. One year after pleurectomy and having discontinued methysergide all biochemical tests were normal.

Biopsy↗

PubMed1988

Effects of intrathecal administration of methysergide, phentolamine, and pindolol on pressor responses to electrical stimulation of the rostral ventrolateral medulla.

Neurons projecting from the rostral ventrolateral medulla (RVLM) to the spinal cord are important in blood pressure control. The present experiments examined the role of spinal adrenoreceptors and serotonin receptors in mediating the pressor effects of electrical stimulation of the RVLM. Accordingly the effects on blood pressure of electrical stimulation of the RVLM were studied before and after intrathecal administration of adrenergic or serotonergic antagonists in normotensive and hypertensive rats. Electrical stimulation in the area of the RVLM-B3 serotonin-containing neurons in Wistar-Kyoto (WKY) rats increased blood pressure, and the pressor responses were reduced by intrathecal methysergide (30 and 100 micrograms). Similar findings were seen in spontaneously hypertensive rats (SHR). In WKY, electrical stimulation in the area of the RVLM-C1 epinephrine-containing neurons, increased mean arterial pressure (MAP), but the pressor responses were unaffected by intrathecal phentolamine (15 micrograms), pindolol (2 micrograms), or methysergide (30 and 100 micrograms), or saline. The results suggest that the pressor effects of stimulation of the RVLM-B3 area are mediated at least in part through activation of spinal serotonin receptors. The lack of effect of phentolamine and pindolol on the RVLM-C1 area pressor responses raises a question regarding the importance of spinal adrenergic receptors in mediating these effects.

Animals↗

PubMed1985

Effect of topically applied atropine, methysergide and chlorpheniramine on nasal challenge with serotonin.

Serotonin challenge in the nose produces sneezing and rhinorrhoea. To study the mode of action of serotonin in the nose, 14 normal persons, in a double-blind, randomized study, were provoked with serotonin in three concentrations. Fifteen minutes before challenge, they were pretreated in the nose with either a cholinoceptor antagonist (atropine), a serotonin antagonist (methysergide), an H1-histamine antagonist (chlorpheniramine) or isotonic saline. The number of sneezes was noted, and the amount of secretions measured. Serotonin induced dose-related increase in sneezing and hypersecretion (P less than 0.02). Atropine pretreatment reduced the amount of secretion (P less than 0.05 and P less than 0.1), but had no effect on sneezing. Methysergide and chlorpheniramine had no effect on the serotonin-induced nasal symptoms. Unilateral challenge with serotonin induced secretions from both sides, suggesting that serotonin-induced nasal symptoms are partly reflex-mediated.

Adult↗

PubMed1978

Retroperitoneal fibrosis, methysergide and malignant lymphoma.

A patient who developed retroperitoneal fibrosis on low dose continuous methysergide therapy is presented. Discontinuing the drug led to rapid clinical improvement but the patient was subsequently found to have disseminated malignant lymphoma. This may have had a synergistic effect with methysergide in producing retroperitoneal fibrosis. The patient had also previously had thyrotoxicosis but no evidence of a continuing autoimmune process was found.

Antineoplastic Agents↗

PubMed1981

Reactivity of isolated trachea, bronchus and lung strip of cats of carbachol, 5-hydroxytryptamine and histamine: evidence for the existence of methysergide-sensitive receptors.

1 The reactivity was investigated of cat isolated tracheal chains, bronchial spirals and lung parenchymal strips to carbachol, 5-hydroxytryptamine (5-HT) and histamine. 2 Carbachol and 5-HT produced concentration-dependent contractions of all three tissues, responses to the former drug being selectively blocked by atropine and to the latter by methysergide. 3 Histamine failed to elicit a contractile response from the tracheal or bronchial muscle. However, it induced dose-related concentrations of the lung strips, that were selectively blocked by mepyramine. 4 It is concluded that lung parenchymal strips of cats possess mepyramine-sensitive histamine H1-receptors. Receptors for 5-HT, susceptible to methysergide, occur in the tracheobronchial smooth muscles as well as in lung strips of cats.

Animals↗

PubMed1990

Heterogeneity of alpha 2-adrenoceptors in rat cortex but not human platelets can be defined by 8-OH-DPAT, RU 24969 and methysergide.

1. Saturation experiments indicated that [3H]-yohimbine binding was specific, saturable and labelled a single population of sites in rat cerebral cortex (Kd 5.3 +/- 0.9 nM, Bmax 121 +/- 10 fmol mg-1 protein) and human platelets (Kd 0.7 +/- 0.1 nM, Bmax 152 +/- 10 fmol mg-1 protein). 2. The alpha 2-adrenoceptor antagonists, yohimbine, rauwolscine, WY 26703, idazoxan and BDF 6143 displaced [3H]-yohimbine binding to each tissue in a simple manner, with high affinity and Hill slopes close to unity. 3. The alpha 1-adrenoceptor agonist, oxymetazoline and the antagonist prazosin inhibited the binding of [3H]-yohimbine to rat in a complex manner consistent with an interaction at more than one site. However, indoramin and WB 4101 only appeared to interact with one site. In contrast, in human platelets, all antagonists gave rise to monophasic displacement curves with Hill slopes close to unity suggesting a single site of interaction. 4. The 5-hydroxytryptamine (5-HT) receptor ligands, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), RU 24969, and methysergide inhibited the binding of [3H]-yohimbine to rat cortex with high and low affinity, consistent with an interaction with two populations of binding sites. However, inhibition of [3H]-yohimbine binding to human platelets suggested a single site of interaction. The low affinity of 5-HT, 5-carboxyamidotryptamine (5-CT) and dipropyl-5-CT indicated that [3H]-yohimbine was not labelling a 5-HT1-like site in rat cortex. 5. The ability of 8-OH-DPAT, RU 24969 and methysergide in addition to prazosin and oxymetazoline to differentiate [3H]-yohimbine binding provides additional pharmacological evidence for heterogeneity within rat cortical alpha 2-adrenoceptors. However, if the two sites in rat cortex that are differentiated by the 5-HT ligands represent (alpha 2A- and alpha 2B-adrenoceptor subtypes as defined by prazosin and oxymetazoline, then they do not correspond to the population of sites in human platelets. As receptor classification should be linked to affinity of drugs rather than tissue distribution, the current classification of alpha 2-adrenoceptor subtypes does not appear to be satisfactory.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMedDate not supplied

Treatment of infantile spasms with methysergide and alpha-methylparatyrosine.

Twenty-four newly diagnosed and previously untreated infantile spasm patients were treated for 3 weeks with either methysergide (12 patients) or alpha-methylparatyrosine (12 patients). Response to therapy was determined objectively with 24-h polygraphic/video monitoring techniques and was defined as cessation of spasms and disappearance of the hypsarrhythmic EEG pattern. Two (17%) of the patients treated with alpha-methylparatyrosine responded to therapy, and one (8%) of the methysergide-treated group showed a response.

Adrenocorticotropic Hormone↗

PubMed1977

Effect of methysergide and indomethacin on the anaphylactic contraction of the rat isolated uterus (Schultz-Dale response).

The anaphylactic contraction (Schultz-Dale response) of the isolated uterus from actively sensitized rats was partially suppressed by methysergide, 1.5 mug/ml. Although the inhibitory effect of indomethacin, 3.5 mug/ml, was only slight, the combination of indomethacin and methysergide abolished the response almost completely. These observations indicate that, although serotonin must be the primary mediator of tha anaphylactic uterine response, prostaglandin is also involved. Metiamide, a histamine H2-receptor antagonist, 10 mug/ml, did not affect the anaphylactic response, suggesting that histamine was not released in amounts sufficient to counteract the uterine contracting mediators.

Anaphylaxis↗

PubMed1975

Inhibition of drug-induced anorexia in rats by methysergide.

Iproniazid was found to reduce food consumption in fasting rats. Combined treatment of iproniazid with tryptophan resulted in a significantly greater anorexic action whilst tryptophan alone had no effect on food consumption. Iproniazid treatment was associated with a significant increase in brain 5-hydroxytryptamine (5-HT) concentration but in association with tryptophan higher brain 5-HT concentrations were recorded. The anorexic action of the iproniazid-tryptophan combination was antagonized in a dose-dependent fashion by methysergide. Equivalent levels of anorexia induced by fenfluramine and mazindol were similarly antagonized by methysergide in a dose-related manner. The results suggest a common role of 5-HT in the inhibition of eating behaviour in fasting rats when anorexia is induced by iproniazid, fenfluramine or mazindol, sensitive to a specific 5-HT antagonist.

Animals↗

PubMed2005

Psychiatric side effects during methysergide treatment.

A patient is reported with psychological change characterised by impaired concentration and thought projection, followed by both severe anxiety and depression, starting after three weeks on high dose methysergide. The acute problem settled slowly after methysergide withdrawal and is likely to represent an unusual and serious side effect of that drug.

Adult↗

PubMed1974

Effects of ergotamine and methysergide on blood platelet aggregation responses of migrainous subjects.

Platelet aggregation responses to 5-hydroxytryptamine (5-HT) were measured in plasma from migrainous subjects taking either methysergide maleate or ergotamine tartrate and were found to be reduced. Blood 5-HT levels of subjects free of headache were not affected by these drugs. The results support the hypothesis that methysergide and ergotamine act by occupying 5-HT uptake sites in vessel walls, leaving 5-HT molecules available to occupy receptors concerned with vasoconstriction.

Blood Platelets↗

PubMed1989

Methysergide-induced psychosis: case report with long-term follow-up.

Methysergide, a congener of LSD and potent serotonin (5-HT) antagonist, induced a florid transient psychosis resembling an LSD psychosis in a patient with spasmodic torticollis with a family history of schizophrenia. Thirteen years later he developed a major depression. A variety of other drug challenges and treatments for his torticollis had no psychotomimetic effect. Blockade of 5-HT receptors may subserve methysergide-induced psychosis.

Adult↗

PubMed1976

Modification of procine stress ulceration by methylprednisolone, vitaminA and methysergide treatment.

Using a swine shock ulcer model, three pharmacological agents, methylprednisolone, vitamin A and methysergide were evaluated, as they protect gastric mucosa against acute ulceration. Following haemorrhagic shock (3 h duration; mean arterial pressure 40 mm Hg) nine of the ten control animals (90%) developed gastric ulceration. Of the six test animals treated with intravenous methylprednisolone during the shock, only one (17%) developed gastric lesions (p less than 0.02; x2 = 5.76). Of the ten test animals pretreated with massive doses of parenteral vitamin A, only three (30%) developed lesions (p less than 0.05; x2 = 5.21). In contrast to this, treatment with methysergide, a serotonin antagonist, did not significantly effect the ulceration rate, since four of the six test animals (67%) had gastric lesions. The results suggest that methylprednisolone and vitamin A do protect the gastric mucosa from experiment stress ulceration, but their mechanism of action remain obscure and further investigation is needed to judge their value in clinical use.

Animals↗

PubMed1977

Methysergide-induced heart disease: a case of multivalvular and myocardial fibrosis.

Methysergide (Sansert) is known to cause mitral and aortic valvular fibrosis and dysfunction, but has generally not been known to damage right heart valves or the myocardium, and cardiac fibrosis has not been considered to be a risk if therapy is intermittently interrupted. The woman who is the subject of this case report developed catheterization-proven severe tricuspid and moderate aortic and mitral regurgitation during noncontinuous therapy with methysergide. In addition, right ventricular endomyocardial biopsy revealed extensive endocardial and intramyocardial fibrosis.

Aortic Valve Insufficiency↗

PubMed1978

Reversal by methysergide of inhibition of insulin secretion by prostaglandin E in the dog.

These studies were designed to examine whether interrelationships exist between serotonin and prostaglandin E (PGE) during regulation of insulin secretion in dogs in vivo. In our studies serotonin was found to inhibit insulin responses to intravenous glucose. This inhibition was not reversed by complete adrenergic blockade provided through combined phentolamine and propranolol pretreatment. This property of serotonin is similar to that of PGE which also inhibits glucose-induced insulin secretion in vivo independently of adrenergic activity. To investigate whether these effects of serotonin and PGE are related, studies with methysergide (a serotonin antagonist) and indomethacin (a PGE synthesis inhibitor) were performed. Methysergide reversed the effects of both PGE and serotonin. In contrast, indomethacin did not diminish the inhibitory effect of serotonin upon insulin secretion. It is hypothesized that endogenous serotonin may play a role in the inhibitory effect of PGE upon insulin secretion in dogs in vivo.

Animals↗