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At least 19 recordsLinked to original sources
PubMed1975

Analysis of ergotamine - 5-HT interaction on the isolated rat stomach preparation.

The effect of ergotamine on the isolated rat stomach and its influence on the response to ACh and 5-HT were investigated. The log dose-response curve of ergotamine was bell-shaped. Extension of the incubation time of ergotamine resulted in a parallel shift to the left of the curve. The response to ergotamine was inhibited by methyserigide and piperoxan. Incubation with ergotamine resulted in a decrease of the pD2-value of 5-HT together with a marked suppression of the maximum of the 5-HT curve. The response to ACh was affected in accordance with the prediction of an action of ACh and ergotamine on different receptors. The prolonged receptor stimulation by 5-HT or ACh resulted in a decrease of the apparent affinity towards their receptors. Incubation with ACh resulted in a parallel shift to the right of the 5-HT curve. However no inconsistency with the theoretical prediction of an action on separate receptors was observed with the ACh curve in the presence of 5-HT. It is concluded that ergotamine is a partial agonist on the D-tryptamine receptors of tbe isolated rat stomach. The marked decrease of the maximum of the 5-HT curve by ergotamine is probably caused by the slowly reversible character of its antagonism. The parallel shift to the left of the ergotamine curve with the extension of the incubation time and the persistence of its antagonism both are probably caused by a slow diffusion into and from the biophase.

Acetylcholine↗
PubMed1992

Comparative effects of the antimigraine drugs sumatriptan and ergotamine on the distribution of cardiac output in anaesthetized pigs.

The haemodynamic effects of sumatriptan, a 5-HT1-like receptor agonist, and ergotamine, an agonist at alpha-adrenergic, dopamine as well as 5-HT receptors, were compared using intracardiac injection of radioactive microspheres of different sizes in anaesthetized pigs. Ergotamine (0.02 mg.kg-1) and sumatriptan (0.3 mg.kg-1) decreased systemic vascular conductance and cardiac output. Only ergotamine raised arterial blood pressure. Both sumatriptan and ergotamine decreased arteriovenous anastomotic, but not capillary, blood flow in the head and body skin. Arteriovenous and capillary blood flow in the dura mater and nasal mucosa and capillary blood flow in the brain, kidneys, adrenals, intestine, heart, spleen and muscle remained unchanged. However, kidney conductance was decreased by both drugs, spleen conductance by sumatriptan and heart, liver and adrenal conductances were decreased by ergotamine. Thus, both sumatriptan and ergotamine constricted arteriovenous anastomoses in the skin, but not in the dura mater or nasal mucosa. Ergotamine constricted the vasculature more than sumatriptan, although both drugs may differentially decrease vascular conductances in some organs.

Anesthesia↗
PubMed1978

The effect of ergotamine on tissue blood flow and the arteriovenous shunting of radioactive microspheres in the head.

1 The radioactive microsphere method was used to study the effects of ergotamine (5, 10 and 20 mug/kg, i.v.) on systemic and regional haemodynamic variables in chloralose-urethane anaesthetized cats. The influence of the drug was also studied on the number of 15 mum microspheres escaping entrapment in the head to emerge in the left external jugular vein.2 Ergotamine decreased the heart rate and cardiac output. Since arterial blood pressure remained unchanged, calculated total peripheral resistance increased.3 The regional distribution of cardiac output obtained with 15 mum microspheres agreed well with previous studies in cats where 25 mum spheres were used. The most pronounced difference was that in the present investigation more microspheres, apparently escaping through arteriovenous anastomoses (AVAs), were detected in the lungs than when larger spheres had been used.4 Coronary blood flow decreased, while uterine blood flow was increased by the drug. The microsphere content of the lungs, which receive the spheres not only via bronchial arteries but also via AVAs, was greatly reduced by all doses of ergotamine. Ergotamine did not influence tissue blood flow to other major organs such as the brain, kidneys, skin, liver, skeletal muscle or the gastrointestinal tract.5 In the 16 experiments, 0.46 +/- 0.05 (s.e. mean)% of the total microspheres injected (equivalent to 11.7 +/- 1.4% of microspheres detected in the left-side of the head) appeared within 2 min of microsphere injection into the left external jugular vein. The highest dose of ergotamine significantly reduced the shunting of the microspheres in the head.6 Since 15 mum microspheres are only likely to reach the lungs by passing into the venous circulation through large glomus-type AVAs, we conclude that ergotamine reduces the fraction of microspheres appearing in the lungs by causing strong vasoconstriction in the AVAs in the head.7 In conformity with the closure of head AVAs is the finding that ergotamine reduced the jugular venous Po(2) and O(2) saturation thereby increasing the A-V O(2) saturation difference.8 It is quite possible that decreased A-V shunting may be the prominent mechanism of the antimigraine action of the drug, since sudden opening of AVA's has been implicated in the pathophysiology of migraine-syndrome.

Animals↗
PubMed1979

Systemic availability of ergotamine tartrate after oral, rectal and intramuscular administration.

Plasma ergotamine levels were measured in 33 volunteers (subgroups 11, 12 and 10) after a single dose of ergotamine administered by various routes. Ergotamine tartrate was given in doses normally used in the treatment of acute migraine--2.0 mg orally, 2.0 mg combined with 100 mg caffeine rectally and 0.5 mg i.m. Plasma ergotamine concentrations were determined by radioimmunoassay. The highest and longest lasting levels were found after i.m. administration, the peak concentration being 1.94 +/- 0.34 (SEM) ng/ml at 1/2 h. The corresponding maximum concentrations after oral and rectal administration were 0.36 +/- 0.08 ng/ml at 2 h and 0.42 +/- 0.09 ng/ml at 1 h. In most of the subjects the plasma ergotamine level began to rise again at 24 to 48 h. The cause of the elevation is not known but it might favour possible accumulation of the drug. Absorption from suppositories was at least as good as after oral administration and the former route may therefore be advantageous for migraine patients in whom nausea and vomiting during an attack may prevent efficient oral medication.

Administration, Oral↗
PubMed1979

Presynaptic inhibition by ergotamine of the responses to cardioaccelerator nerve stimulations in the cat.

The effects of ergotamine on the tachycardia elicited by postganglionic stimulation of the cardioaccelerator nerve have been investigated in both intact and spinal (desmethylimipramine-pretreated) cats. Ergotamine (2.5--20 microgram kg-1) selectively antagonized the response to low-frequency (0.3--3 Hz) stimulation. The responses elicited by stimulation of the nerve with higher frequencies (greater than 10 Hz) either remained unaltered or were facilitatated by the drug. Pretreatment of the cats with pimozide (0.2 mg kg-1) completely antagonized the inhibitory effects of ergotamine on the sympathetic neuron. Although phentolamine (0.5 mg kg-1) did appear to attenuate the effects of ergotamine, the changes were, however, not statistically significant. Since the drug did not reduce the cardiac effects of isoprenaline or tyramine, it is concluded that ergotamine interferes with the release of noradrenaline from the cardioaccelerator nerve, mainly by stimulating the presynaptic dopaminergic receptors. This effect may be an important mechanism by which the drug causes bradycardia in almost all species regardless of the blood pressure response.

Animals↗
PubMed1976

Quantitative thin-layer chromatographic analysis of ergotamine tartrate and caffeine in the nanogram range.

Direct, quantitative, thin-layer chromatographic methods for the determination of ergotamine tartrate and caffeine in the presence of each other in blood and in pharmaceutical preparations are described. The blood is centrifuged, the plasma decanted from the coagulum and deproteinized with acetone-methanol. After removal of the solvent mixture, the active ingredients are extracted from the remaining aqueous solution with chloroform. In the case of the pharmaceutical preparations, the active ingredients are also extracted with chloroform or methanol. Ergotamine tartrate and caffeine are separated on pre-coated silica gel 60 F254 plates and measured directly on the thin-layer plate, ergotamine tartrate being determined by the fluorescence method, excitation wavelength 365 nm, at lambdamax.=450 nm and caffeine by the reflactance method at lambdamax.=274 nm. The analytical methods are suitable for the bioavailability studies of these drugs in blood as they enable the determination of 20 ng ergotamine tartrate with a coefficient of variation of 6.7% and the determination of 200 ng caffeine with a coefficient of variation of 6.1%. The methods have also proved useful in the determination of the active ingredients of drug forms such as tablets and suppositories and can be well reproduced with a maximum coefficient of variation of 4.9% for ergotamine tartrate and 3.5% for caffeine.

Biological Availability↗
PubMedDate not supplied

Regional myocardial perfusion and wall thickness and arteriovenous shunting after ergotamine administration to pigs with a fixed coronary stenosis.

The hemodynamic effects of antimigraine drug ergotamine, which is considered contraindicated in patients with coronary artery disease, were studied in pigs with a normal myocardial circulation (doses of 8, 16, and 32 micrograms/kg, i.v.) or with acute coronary stenosis (8 micrograms/kg). In both groups of animals, ergotamine decreased heart rate, cardiac output, and arteriovenous anastomotic blood flow while increasing aortic blood pressure and systemic vascular resistance. No effects on total ventricular blood flow and its distribution within the myocardium were found in normal animals. In animals with a clamp on the left anterior descending coronary artery (LAD), the blood flow to the LAD-perfused area was reduced from 1.10 +/- 0.16 to 0.67 +/- 0.05 cm3/min/g. The endocardium was affected more than the epicardium and the endo/epi flow ratio decreased from 1.18 +/- 0.05 to 0.74 +/- 0.07. Ergotamine increased the blood flow to the ischemic zone towards normal values, and the endo/epi flow ratio to 1.05 +/- 0.21. However, myocardial wall thickness parameters, which showed functional deterioration during ischemia, did not change after ergotamine. The present study provides no clear support for cardiovascular contraindications to ergotamine administration.

Animals↗
PubMed1976

Evidence for stimulation of 5-HT receptors in canine saphenous arteries by ergotamine.

Changes in tension of spiral strips from dog saphenous arteries were monitored isometrically. Dose-response curves for noradrenaline, 5-HT and ergotamine were established without and after a 30 min incubation with phentolamine or pizotifen. Phentolamine was about 15 times more potent in antagonizing responses to noradrenaline (pA2 value=7.4) than those to 5-HT (pA2 value=6.2) but it was nearly equipotent in antagonizing responses to ergotamine (pA2 value=6.5) and those to 5-HT. Pizotifen was about 500 times less potent in antagonizing noradrenaline effects than 5-HT but again nearly equipotent when tested against ergotamine and 5-HT. It is suggested that in canine saphenous arteries the stimulant activity of ergotamine is mediated mainly through 5-HT receptors.

Animals↗
PubMed1979

Effect of ergotamine on cranial arteriovenous shunting in experiments with constant flow perfusion.

The effect of the antimigraine drug, ergotamine, was studied on the distribution of flow throughout the cranial microcirculation of the cat, using microspheres suitable in size to separate capillary flow from flow through the arteriovenous anastomoses. A constant flow perfusion experiment was used in order to eliminate the secondary effect of ergotamine on the microcirculation through a reduction in carotid blood flow per se. Under the experimental conditions, ergotamine decreased in a dose-dependent way the fraction of perfusion flow shunted through the arteriovenous anastomoses. This mode of action of ergotamine sheds new light on the so-called migraine shunt theory.

Animals↗
PubMed1992

Long-term ergotamine abuse: effect on adrenergically induced mydriasis.

The mydriatic action of sympathomimetic eyedrops after a therapeutic dose of ergotamine was measured in migraine patients with and without histories of long-term ergotamine abuse. Mydriasis induced by the postsynaptic alpha 1-agonist phenylephrine was similar in both groups of patients tested, whereas pupillary dilation caused by the release of noradrenaline tyramine was markedly greater in patients with histories of ergotamine abuse. The enhanced response to tyramine disappeared after drug withdrawal. These findings indicate that continuous ergotamine medication causes a reversible alterations in iris sympathetic transmission. This manifestation may reflect a central inhibition of pupillary sympathetic activity.

Adult↗
PubMed1975

Enhanced prostaglandin synthesis contributes to the venoconstrictor activity of ergotamine.

Spiral strips from dog saphenous veins were contracted by 2.5 X 10(-9) M ergotamine, a concentration giving about 50% of maximal response. Phentolamine (3.6 X 10(-6) M) reduced these effects by 60% and indomethacin (2.8 X 10(-7) M) by 30%. Indomethacin was more effective in reducing ergotamine-induced increase of prostaglandin E-like activity in the bathing fluid than those induced by noradrenaline or potassium chloride. Arachidonic acid was more effective in increasing tension in ergotamine-stimulated than in noradrenaline- or potassium-stimulated veins. These findings suggest that the long-lasting venoconstrictor activity of ergotamine is mediated mainly by alpha-adrenoceptors but that enhanced formation of prostaglandin E-like substance(s) may also contribute.

Animals↗
PubMed1976

Determination of the content and purity of ergotamine preparations by means of high-pressure liquid chromatography.

A reversed-phase system of high-pressure liquid chromatography with solvent gradient is described for testing the purity of ergotamine as an active substance and for checking its concentration in pharmaceutical preparations. Because of its good resolution, this system can be used not only for the selective assay of ergotamine but also for the identification and quantitative determination, in the same chromatogram, of seven known isomerization and hydrolysis breakdown products. Simultaneous detection at two different UV wavelengths also makes it possible to measure further breakdown products formed by addition at the 9,10 double bond (lumi-compounds). The advantages of the system lie in the determination of all of the products within ca. 20 min, direct injection of low-dosage injection solutions and sensitive detection of polar breakdown products. The system is reproducible with regard to retention times and quantitative determination. It is suitable as a quality-control method for the routine determination of the content and purity of ergotamine preparations.

Chromatography, High Pressure Liquid↗
PubMed1992

Lack of effect of the antimigraine drugs, sumatriptan, ergotamine and dihydroergotamine on arteriovenous anastomotic shunting in the dura mater of the pig.

1. In anaesthetized animals, the antimigraine drugs, sumatriptan, ergotamine and dihydroergotamine, reduce carotid arteriovenous anastomotic shunting. Within the carotid vascular bed arteriovenous anastomoses are located, amongst other places in the dura mater, which is a putative site of the pain during a migraine attack. 2. In this investigation, we have localized and measured the arteriovenous shunting within the carotid vascular bed of the pig by using simultaneous intracarotid injections of radiolabelled microspheres of three different sizes (10, 15 and 50 microns), which provides an index of blood flow via arteriovenous anastomoses larger than approximately 14, 27 and 90 microns diameter, respectively. The effects of sumatriptan (0.3 mg kg-1), ergotamine (0.02 mg kg-1), dihydroergotamine (0.1 mg kg-1) and saline were studied by repeating the injections of 15 and 50 microns spheres after the treatments. 3. There was no difference in shunting or entrapment between the 10 and 15 microns microsphere, indicating the absence of arteriovenous anastomoses with a diameter between 14 and 27 microns. 4. Arteriovenous anastomoses with a diameter between 27 and 90 microns, as indicated by the difference in blood flow measured by 15 and 50 microns spheres, were located in the dura mater, ears, skin, fat and, to a lesser extent, in the skeletal muscles and eyes. 5. Sumatriptan, ergotamine and dihydroergotamine reduced the overall flow in the smaller arteriovenous anastomoses (diameter between 27 and 90 microns), and even more in larger shunts (wider than 90 microns). 6. Locally, blood flow in the smaller arteriovenous shunts was reduced in the skin and fat, but not in the dura mater, ears, eyes and muscles.It is not possible to determine in which tissues blood flow in the larger arteriovenous anastomoses was reduced.7. Tissue blood flow measured with 15 gm microspheres remained unchanged after the three antimigraine drugs, implying a lack of effect on capillary flow.8. It is concluded that in the anaesthetized pigs the only evident effect of these antimigraine drugs on carotid haemodynamics is a decrease in blood flow in both smaller and larger arteriovenous anastomoses;the smaller arteriovenous anastomoses were affected in the skin and fat, but not in other tissues.

Animals↗
PubMedDate not supplied

Ergotamine and cerebral blood flow.

We measured the cerebral blood flow (CBF) of 16 patients by the xenon-133 intracarotid method before and after the intramuscular injection of ergotamine tartrate. The regional and hemispheric CBF was unaltered, even in 3 migraneurs in who ergotamine relieved the headache. Ergotamine tartrate in therapeutic doses has no effect on the cerebral circulation.

Adult↗
PubMed1992

Ergotamine: its use in the treatment of migraine and its complications.

This paper gives a review of the use of ergotamine in the treatment of migraine and discusses its side effects and the treatment of possible complications. It is concluded that ergotamine is an effective and valuable substance in the treatment of acute attacks of migraine. However, ergotamine remains a potentially dangerous substance, its possible side effects being multiple and in some cases very serious. In view of the important adverse effects, the further study of other molecules effective in the treatment of acute migraine attacks is warranted.

Autonomic Nervous System Diseases↗
PubMedDate not supplied

Anterior tibial compartment syndrome associated with ergotamine ingestion.

This is the first reported case of acute anterior tibial compartment syndrome following ergotamine tartrate overdosage. A 25-year-old man developed signs and symptoms of ergotism after ingestion of 72 mg of ergotamine tartrate over the 12 days prior to his hospital admission. On the fourth hospital day, the patient developed bilateral anterior tibial compartment syndrome. The development of this syndrome is postulated to have been due to the progressive edema and tissue pressure in the anterior tibial compartments, worsened by the gradual improvement of the peripheral circulation which followed the diminished vasopastic effect of the ergotamine.

Adult↗
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↗
PubMed1979

Tolfenamic acid is as effective as ergotamine during migraine attacks.

Tolfenamic acid (a potent inhibitor of prostaglandin biosynthesis), ergotamine tartrate, acetylsalicylic acid, or placebo was administered during 160 migraine attacks in twenty women in a double-blind, cross-over study. Tolfenamic acid and ergotamine were equally effective in reducing the duration and intensity of attacks, but side-effects, especially nausea, were less common with tolfenamic acid. This probably accounted for the patients' preference for tolfenamic acid. The effectiveness of tolfenamic acid in acute migraine attacks accords with the postulated role of prostaglandins in migraine.

Adolescent↗