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At least 235 records · Page 13Linked to original sources
PubMed1996

Platelet activation during provocation of coronary artery spasm by ergonovine and cold pressor testing in patients with angina pectoris.

The role of coronary spasm in variant angina is well established. We have studied the time course of platelet activation during Ergonivine provocation to determine one significance of platelet indices for spasm testing. The results showed that spontaneous platelet aggregates and beta-thromboglobulin levels in patients with coronary vasospasm were increased during provocation and that platelet activation during a positive Ergonivine test precede ECG changes and chest pain.

Adenosine Diphosphate↗
PubMed1960

Effects of ergometrine (ergonovine) on the isolated atherosclerotic heart of the cholsterol-fed rabbit.

Ergometrine usually depresses the S-T segment as in coronary insufficiency, when injected intravenously in rabbits with experimental coronary atherosclerosis and in patients with effort angina, but not in normal animals and man. To explain this difference, we carried out Langendorff perfusion studies in 32 normal and 29 atherosclerotic isolated rabbit hearts. Preliminary tests with ergometrine were done to ensure that advanced coronary atherosclerosis had developed in the rabbits fed a cholesterol diet; pathological examination of the heart after perfusion confirmed the result of the final test with ergometrine. Before drugs were perfused, the basal rate of coronary flow was greater, the heart rate was slower and the contractile amplitude was smaller in the atherosclerotic than in the normal hearts; nitroglycerin markedly increased flow in both normal and atherosclerotic groups. Ergometrine consistently caused a reduction in contractile amplitude with negligible changes in heart rate in both normal and atherosclerotic hearts. On coronary flow, however, the effects of ergometrine differed significantly in these groups; in doses of between 0.2 and 0.4 mg., the average decrease in flow was 8% in normal and 22% in atherosclerotic hearts. The effect was more variable in normal hearts and an increase in flow sometimes occurred. The difference in the response of normal and atherosclerotic hearts was particularly striking when ergometrine was given during recovery from a reduction of coronary flow which had been induced by vasopressin. Ergometrine then uniformly increased flow in the normal, but usually had the opposite effect in the atherosclerotic heart. In normal and atherosclerotic hearts, cardiac effects of vasopressin were similar. Tachyphylaxis to vasopressin, but not to ergometrine, was observed.

Angina Pectoris↗
PubMed1988

Agonist profile of ergometrine (ergonovine) on a population of postsynaptic alpha-adrenoceptors.

Ergometrine (0.02-5 microM) produced concentration-related contractions of the mouse anococcygeus muscle, which were unaffected by cocaine (2 microM) or by pretreatment of mice with 6-hydroxydopamine. Contractions were reduced by alpha-adrenoceptor antagonists; the rank order of potency was prazosin greater than phentolamine greater than yohimbine. With phenoxybenzamine as antagonist, the estimated dissociation constant (KD) for ergometrine was 0.41 microM. It is concluded that ergometrine causes direct activation of postsynaptic alpha 1-adrenoceptors, and it is suggested that it acts on the same subtype of the receptor as imidazoline agonists.

Adrenergic alpha-Antagonists↗
PubMed1987

Oral isosorbide 5-mononitrate can protect from myocardial ischemia induced by ergonovine test and by isometric effort. Preliminary results from an echocardiographic acute study in anginal patients.

Isosorbide 5-mononitrate (IS 5-MN) has favourable pharmacodynamic properties, such as the specific half-life (close to 5 h) and the bioavailability (100% after oral ingestion). The efficacy of IS 5-MN (20 mg t.i.d.) in the treatment of stable angina has been documented in previous studies. In the present acute study, two subsets of patients were evaluated: the first group consisted of 10 patients with coronary vasospasm in whom oral IS 5-MN was effective in preventing myocardial ischaemia due to an abrupt reduction in coronary blood flow; the second group regarded 8 patients with a mixed form of angina, where the responsible mechanism for ischaemia can be considered a combination of increased myocardial oxygen demand and reduction of coronary blood flow due to vasoconstriction of large vessels. In all these patients, IS 5-MN was able to protect against transient myocardial ischaemia induced by isometric test. In conclusion, from the data available in our studies, IS 5-MN appears to be a useful drug in anginal patients: the beneficial effect is likely based on its capability both to prevent the abnormal vasoconstriction of diseased coronary vessels and to reduce myocardial oxygen demand.

Administration, Oral↗