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At least 19 recordsLinked to original sources

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↗

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↗

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↗

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↗

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↗

PubMed1976

[Treatment of orthostatic hypotension with dihydrated ergotamine derivatives].

After a brief review on the orthostatic disturbances in the regulation of blood circulation the author stresses upon the treatment of the orthostatic hypotonia with dihydrated ergotamine derivatives (Dihydergot retard). A favourable effect was obtained in 59 patients (84.3%) out of the treated 45 patients with secondary orthostatic hypotonia and 25 patients with primary hypotonia. The treatment of orthostatic hypotonia with dihydrated ergotamine derivatives was emphazised to be pathogenetically grounded, because tones the venous system (system of low pressure) and eliminates the developed contraregulatory sympathicotonia. Its combination with low doses of sympathominetics improves even more the effect.

Adolescent↗

PubMed1979

Ergotism with therapeutic doses of ergotamine tartrate.

Two cases of acute ergotism are described in patients taking therapeutic oral doses of ergotamine tartrate and concomitant triacetyloleandomycin. Both showed satisfactory response to infusion of sodium nitroprusside with normal perfusion being obtained in the affected limbs. The treatment of ergotism with sodium nitroprusside is reviewed and the apparent interaction of ergotamine and triacetyloleandomycin is discussed.

Adult↗

PubMed1977

Analytical problems with putrefaction in a fatal case involving ergotamine and pentazocine.

A 29-year-old male drug addict was found dead at the bottom of a staircase. Analysis of the acid-hydrolized blood showed the presence of pentazocine and two characteristic compounds that contained L-phenylalanine and D-proline, linked together by peptide bounds. It was shown that the latter two components could emanate from the peptide part of ergotamine under the conditions used. It seemed likely that, at the time of analysis, pentazocine and ergotamine were present at concentrations far above therapeutic values. A third component in the blood could not be identified.

Adult↗

PubMed1978

[Bilateral vascular papillitis following ergotamin medication (author's transl)].

A 36-years aged woman suffering from migraine used Ergosanol special-suppositories. An edema of the retina with star figure appeared in both eyes with only a few months distance. After putting away that drug visual acuity restituted completely in spite of a partial neuritic atrophy of the optic nerve in the first suffering eye. If Ergotamin containing drugs are not used for too long time the condition usually is getting better within a few days. Thereby the diagnosis can be confirmed clinically. The same results could be expected if DHE leads to Ergotismus which is not yet confirmed. In literature central scotomas as well as annular scotomas are reported. In Ergotamin induced angioneuropathies there is a large difference in individual response. Our observation showed that drugs taken for years are no more felt as a pharmacon by a patient and therefore are not reported to the examinating physician.

Adult↗

PubMed1976

[Ergotamine abuse and retroperitoneal fibrosis (author's transl)].

A case of Ergotamine abuse causing considerable fibrotic changes of the abdominal aorta and iliac vessels and of the retroperitoneal space is reported. Histological and pathogenetic aspects of the arterial changes and the retroperitoneal fibrosis are discussed. They are referred to the permanent constriction of the Vasa vasorum by Ergotamine.

Adult↗

PubMed1976

Responsiveness of isolated canine cerebral and peripheral arteries to ergotamine.

Changes in tension of spiral strips from dog saphenous, external carotid and basilar arteries were monitored isometrically. Serotonin (5-HT) contracted the 3 arterial preparations in about the same concentration range. Compared with noradrenaline (NA) (100%) the efficacy of 5-HT was about 60% on saphenous, 150% on external carotid and about 500% on basilar arteries. Ergotamine (E) stimulated the 3 vascular preparations in concentrations about 100 times lower than 5-HT. Compared with NA the efficacy of E was about 20% on saphenous, 50% on external carotid and 200% on basilar arteries. Compared with 5-HT (100%) however, E had similar constrictor activities in the 3 arteries. It seemed likely therefore that 5-HT receptors are involved in the vasoconstrictor activity of E. Evidence for this was obtained in experiments in which cyproheptadine (Cy), a 5-HT antagonist, was used. For antagonism of E concentrations of Cy about 6 times higher than those required to inhibit 5-HT were necessary, whereas for antagonism of NA about 500 times higher Cy concentrations were necessary. The results suggest that on canine arterial vascular smooth muscle the constrictor activity of E is mediated mainly through serotoninergic receptor sites.

Animals↗

PubMedDate not supplied

Failure of ergotamine to act as an amplifier of sulfonylurea-stimulated insulin secretion.

Normal dogs were injected i.v. with 0.25 mg/kg sodium salt of HB 419 (glibenclamide) and plasma insulin concentrations were measured over a period of 2 hrs. When the animals were given a single i.v. injection of 0.2 mg/kg dihydroergotamine tartrate (DHE) 30 min prior to the administration of HB 419, the insulinogenic effect of the sulfonylurea was considerably amplified (192 muU/ml vs 34 muU/ml at 45 min). No augmentation of the insulinogenic effect of HB 419 was observed when the same experiments were conducted with 0.05, 0.025 or 0.01 mg/kg ergotamine tartrate. At the dose level of 0.1 mg/kg the insulinogenic effect of HB 419 was suppressed. Since the structural difference between these two ergot alkaloids consists of the presence or absence of the double bond at C9 and C10 of the lysergic acid moiety, it appears that saturation of this double bond is an essential structural requirement for DHE to function as an amplifier of sulfonylurea-stimulated insulin release.

Animals↗