Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ergometrine can evoke coronary spasm in patients with variant angina. The cause of ergometrine-induced chest pain in the absence of coronary spasm is not clear. To determine whether ergometrine produced esophageal dysfunction and chest pain, we evaluated 28 patients by esophageal manometry. Six had chest pain in response to ergometrine during cardiac catheterization (group I) and 22 did not (group II). Results of cardiac catheterization were normal in all patients. Seven volunteers with no history of chest pain formed a control group (group III). Esophageal manometry was performed before and after ergometrine administration (0.4 mg I.V.). Ergometrine provocation during esophageal manometry caused significant deterioration in esophageal motility associated with familiar pain in 5/6 group 1 patients. The motility disorders were characterized by repetitive contracts of high amplitude and long duration in the distal esophagus. No patient from group II or III experienced chest pain after ergometrine and only 2 from group II developed long duration contractions. Thus, we conclude that in patients with normal coronary angiograms, ergometrine-induced chest pain without associated coronary spasm suggests that esophageal motility disorders originate chest pain.
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PMID:The ergometrine test: effects on esophageal motility in patients with chest pain and normal coronary arteries. 359 99

Studies were performed on isolated canine coronary artery segments to characterize the mechanism of the constrictor response of ergometrine (ergonovine), an agent used to induce coronary vasospasm in patients with variant angina. Changes in isometric tension were measured in coronary ring segments suspended in organ baths at 37 degrees C filled with a buffered salt solution. Single concentration-response curves were obtained in each tissue by cumulative addition of agonist. Maximum responses to 5-hydroxytryptamine (5-HT) were greater than for ergometrine or phenylephrine, but ergometrine had the lowest EC50. Alpha adrenoceptor block by prazosin (10 nM) or the irreversible antagonist benextramine tetrahydrochloride did not affect responses to 5-HT or ergometrine. Cyproheptadine and pizotifen (0.1-1 muM) depressed the ergometrine and 5-HT concentration-response curves with no change in the location of the EC50 values. Methysergide (0.01-1 muM) had concentration-dependent constrictor activity which was noncompetitively antagonized by cyproheptadine, but unaltered by benextramine tetrahydrochloride pretreatment. In addition, methysergide competitively antagonized the 5-HT and ergometrine concentration-response curves. Estimates of methysergide pKB values (-log dissociation constant) from computer analysis were 7.9 and 8.0 for the two agonists, respectively. It is concluded that methysergide is a partial 5-HT agonist, but cyproheptadine and pizotifen are noncompetitive 5-HT antagonists. Ergometrine is a potent 5-HT receptor agonist in canine coronary artery with negligable alpha adrenoceptor agonist activity.
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PMID:Ergometrine contracts isolated canine coronary arteries by a serotonergic mechanism: no role for alpha adrenoceptors. 611 72

1. Canine circumflex coronary artery ring segments were contracted in vitro by ergometrine, serotonin, phenylephrine, noradrenaline (with propranolol) and a thromboxane A2 analogue, U46619. 2. Ergometrine was classified as a serotonin agonist since concentration-response curves were competitively inhibited by methysergide but not by alpha-adrenoceptor antagonists. 3. Glyceryl trinitrate (IC50 18.6 nmol/l) relaxed the coronary rings precontracted with serotonin, phenylephrine or U46619. In contrast (+/-)-verapamil (0.1-10 mumol/l) was more effective against serotonin than phenylephrine or noradrenaline and was almost inactive against U46619. 4. In a blood perfused left anterior descending coronary artery preparation external diameter was measured by sonomicrometry. Serotonin, U46619 and ergometrine infusions (i.a.) decreased diameter by up to 18% without causing spasm (zero lumen diameter). Lowering the perfusion pressure from 90 to 60 mmHg increased the fall in diameter during serotonin infusions. 5. The negative inotropic potency of verapamil against noradrenaline induced beta-adrenergic stimulation in guinea-pig left atria was compared with the vasodilator potency of verapamil in noradrenaline constricted dog coronary artery rings. Verapamil was eighteen times more potent in cardiac muscle than in coronary smooth muscle. 6. This apparent tissue selectivity of verapamil was confirmed in anaesthetized dogs where plasma concentrations of verapamil 50-150 ng/ml (in the therapeutic range) lowered blood pressure and heart rate and increased P-R interval without greatly reducing the constrictor response to serotonin in the coronary artery. 7. These studies suggest that inhibition of constrictor responses in large coronary vessels may not be an important site of action of verapamil in patients with variant angina.
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PMID:Verapamil: a selective antagonist of constrictor substances in dog coronary artery: implications for variant angina. 695 74

Ergometrine test was undertaken on the 1--3d day after hospitalization in 49 patients with unstable angina pectoris. Pain or ECG changes were recorded in 90% of patients. Reactions with the rise of the ST segment and changes of the T wave on ECG were interpreted as "spastic" and were seen in 43% of cases. Myocardial infarction supervened during hospitalization in 19% of patients with "spastic reactions", and in 14.3% of other patients. Selective coronarography was performed in 33 patients. During coronarography the local spasm of one coronary artery supervening always at the site of organic stenosis was seen in 10 patients (30%). Spastic reactions in angina pectoris can be elicited relatively frequently, but nonspecific reactions are possible, with low tolerance of haemodynamic shifts caused by ergometrine. In the initial angina pectoris, immediately preceding myocardial infarction ergometrine may cause no reaction. An increased tendency of atherosclerotic coronaries to spasm plays a definite role in the development of unstable angina pectoris, in a part of patients only (or only in a certain phase of its course). Such reactions are not associated with a considerably increased danger of development of myocardial infarction.
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PMID:[Unstable stenocardia: the reaction to ergometrine administration]. 706 86

Oesophageal spasm may mimic the pain of myocardial ischaemia. Forty-two patients who were thought to have angina until investigations failed to show any cardiovascular abnormality, were examined for oesophageal disease. Ergometrine provocation during oesophageal manometry caused significant deterioration in oesophageal motility, associated with familiar pain, in 24 patients. Ten age-matched controls were examined in a similar way and ergometrine produced motility changes in four and pain in two. Six volunteers with coronary artery stenosis and exercise-induced angina did not develop oesophageal motility changes during the pain. Ergometrine provocation is useful in establishing the diagnosis of oesophageal spasm in patients with recurrent angina-like pain but no cardiac abnormality.
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PMID:Diagnosis of oesophageal spasm by ergometrine provocation. 706 41

Ergometrine is currently used as a test for Prinzmetal variant angina, causing specifically a coronary artery spasm in these patients, even if the mechanism of this drug on coronaries is still unclear. In isolated rabbit heart perfused at constant flow the administration of ergometrine at the concentration of 2.2 x 10(-5) M evoked a marked and longlasting increase of coronary resistance which was revealed by a rise in perfusion pressure from 68.2 +/- 12.9 to 124.4 +/- 21.7 (m +/- SD; n=21). This increase appears only with repeated perfusions of the drug and moreover it was not reproducible in the same preparation after its maximal response. The vasoconstriction was not significantly affected either by atropine or mepyramine, but it was strongly reduced by the phenoxybenzamine pretreatment (2.9 x 10(-6) M; n=8). It is evident the role of alpha-adrenergic receptors in ergometrine effect, but our results do not allow to understand its true mechanism, in fact the noradrenaline release can not be completely excluded.
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PMID:[Phenoxybenzamine antagonism of ergometrine-induced increase of coronary artery resistance in rabbits]. 744 41

From June 1990 to March 1993, 9 patients undergoing coronary artery bypass grafting (CABG), 4.4% of all CABG cases at our hospital during this period, had significant perioperative coronary spasm. For 4 patients who underwent CABG before May 1992 (Group 1), preventive and suppressive procedures for the coronary spasm were the addition of diltiazem in the cardioplegic solution and the continuous intravenous infusion of nitroglycerin. Perioperative myocardial infarction (PMI) occurred in all 4 patients in Group 1, with the mean peak MB-CPK of 356 +/- 197 IU/l. One patient had delayed sternal closure because of his unstable hemodynamic status. Thereafter, we changed our protocol as follows: 1) Ergometrine loading (intracoronary infusion) test was performed in all candidates for CABG, aiming at finding out patients with a high risk. And for the high-risk patients, in addition to the measures done in Group 1, 2) intraaortic balloon pumping was performed through the perioperative period, and 3) a pig-tail catheter was dwelled in the Valsalva sinus, through which bolus doses of isosorbide dinitrate were injected frequently in this period. 4) Additionally nifedipine was periodically administered through the nasogastric tube. With these intensive preventive/suppressive measures, the perioperative spasm in 5 patients (Group 2) with variant angina were successfully managed, with no resultant PMI nor operative death (The occurrence of PMI was significantly less frequent in Group 2 than in Group 1, with the p value < 0.05). For patients with variant angina undergoing CABG, combined intensive preventive/suppressive measures for perioperative coronary spasm as listed above proved effective.
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PMID:[Prevention of coronary spasm during and shortly after coronary revascularization in patients with variant angina]. 805 58

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.
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PMID:Effects of ergometrine (ergonovine) on the isolated atherosclerotic heart of the cholsterol-fed rabbit. 1440 56