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PubMed1985

Myocardial ischaemia produced by ergonovine-induced vasoconstriction during preexisting coronary stenosis: experimental conditions for the geometric theory.

Experiments were designed to determine the contribution of active vasomotor tone of a large coronary artery during a preexisting coronary stenosis to the production of myocardial ischaemia. The quantitative relations between ergonovine dose and systemic and coronary haemodynamic and electrocardiographic responses during various degrees of coronary stenosis were evaluated in 55 anaesthetised open-chest dogs. In the absence of coronary stenosis, intracoronary infusion of ergonovine (0.04 to 4 micrograms X min-1) had no systemic or coronary haemodynamic effects. In dogs with coronary stenosis created with intraluminal microballoon occluder, ergonovine produced marked decreases in coronary blood flow and distal coronary pressure followed by a decline in left ventricular dP/dt and ST-elevation in epicardial electrogram in the presence of moderate (28 +/- 1.1 mmHg in pressure gradient) and severe (41 +/- 1.4 mmHg), but not mild (15 +/- 0.9 mmHg) stenosis. These detrimental effects of ergonovine were dependent on its dose as well as the severity of preexisting coronary stenosis. Interventions such as aspirin pretreatment or endothelial denudation did not attenuate the coronary vasomotor response or ergonovine, but pretreatment with nifedipine (3 micrograms X kg-1 iv) prevented this response. Intravenous injection of ergonovine (4 to 15 micrograms X kg-1) in doses relevant to clinical usage during intraluminal obstruction resulted in similar changes in coronary haemodynamics as those of intracoronary ergonovine. In contrast, in dogs with various degrees of coronary stenosis produced with an externally applied constrictor device, ergonovine did not affect systemic and coronary haemodynamics. These experiments demonstrate that normal vasomotion superimposed on moderate and severe pliable coronary stenosis can cause transient myocardial ischaemia, which helps to clarify the conditions to produce myocardial ischaemia according to geometric theory.

Animals↗
PubMed1984

Selective hypercontraction caused by ergonovine in the canine coronary artery under conditions of induced atherosclerosis.

The relationship between the hypercontractile response of the regional coronary artery to ergonovine and induced vascular change after endothelial denudation and a high-cholesterol diet was examined in dogs by arteriographic (in situ) and mechanographic (in vitro) methods. In 15 mongrel dogs, selective endothelial denudation of either the left circumflex coronary artery (LCX) or left anterior descending coronary artery (LAD) was repeated twice 1 month apart by means of coronary arterial catheterization. A high-cholesterol diet (20 g/day) was given thereafter for 3 (n = 15) and 6 (n = 8) months. Although there was no difference in the extent of coronary vasoconstriction between the LAD and LCX before or immediately after endothelial denudation, after intravenous administration of ergonovine a significant augmentation of coronary constriction along the denuded portion was noted arteriographically in the long-term phase (1 to 6 months). At the end of the study in vivo, isometric tension of the strips of the denuded and contralateral intact coronary arteries was measured during the cumulative addition of ergonovine, serotonin, or phenylephrine to the organ bath; agonist responses were standardized by the response to 35 mM KCl. Although the concentration-response relations for phenylephrine (10(-9) M to 10(-5) M) were not significantly different between intact and denuded arteries, responses of the denuded portion to cumulative addition of ergonovine (10(-10) M) or serotonin 10(-9) M to 10(-5) M) exhibited markedly depressed threshold concentrations along with a significantly lowered negative logarithm (pD2) of the dose producing 50% of the maximum effect. The tension developed in the denuded portion was also enhanced over that noted in the contralateral coronary artery during the cumulative addition of ergonovine but not during application of phenylephrine. Thus enhanced constriction documented arteriographically may be derived from the localized hypersensitivity to ergonovine. Microscopically, the endothelial denudation and a long-term high-cholesterol diet resulted in a regional intimal thickening with fibrous proliferation but little lipid deposition. Therefore smooth muscle in atherosclerotic arteries may be hypersensitive to specific agonists such as ergonovine and serotonin in a canine preparation. These results suggest that coronary spasm induced by ergonovine in humans is relevant to the presence of atherosclerotic changes in the vascular wall.

Animals↗
PubMed1984

Ergonovine-induced myocardial ischemia: no role for serotonergic receptors?

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.

Aged↗
PubMed1983

Hyperreactivity of coronary arterial smooth muscles in response to ergonovine from rabbits with hereditary hyperlipidemia.

This study was undertaken to examine the response to ergonovine, an agent used to provoke spastic constriction of large epicardial coronary arteries, to elucidate the responsible underlying mechanism, and to determine the impact of endogenous hyperlipidemia on contractile properties of isolated vessels from different beds. The isolated arteries from both control and Watanabe hereditary hyperlipidemic rabbits (WHHL rabbits) were suspended for recording isometric force in oxygenated Krebs buffer and exposed to agonists and antagonists. In atherosclerotic aortas from WHHL rabbits, the concentration-response relations for ergonovine and serotonin exhibited a marked leftward shift with significantly depressed constrictor threshold concentration and lowered one-half maximally effective concentration values. In coronary arteries with no atherosclerotic lesions detectable macroscopically from WHHL rabbits, the concentration-response relations showed a leftward shift for ergonovine but not serotonin. Coronary contraction evoked by ergonovine was remarkably inhibited by 0.1 microM cyproheptadine and 0.3 microM methysergide, serotonergic antagonists, in both groups. alpha-Adrenergic blockade with 0.1 microM prazosin was effective in inhibiting ergonovine-induced contraction of aortas from control rabbits, but not that of atherosclerotic ones. The constrictor response to ergonovine of atherosclerotic aortas was inhibited by cyproheptadine. The responsiveness to ergonovine of both carotid and femoral arteries from WHHL rabbits with no sclerotic lesions, which was suppressed by prazosin was not different from that of control rabbits. In contrast, the concentration-response relations for phenylephrine in the four different types of arteries did not differ appreciably between the two groups, and the constrictor responses to 20 mM KCl were virtually identical. Thus, aortas and coronary arteries exposed to endogenous hyperlipidemia appear to be hyperreactive to ergonovine mediated by a serotonergic mechanism.

Animals↗
PubMed1991

[Intracoronary administration of ergonovine maleate for detecting vasospastic angina; one dose method].

Coronary spasm is an important etiologic mechanism in the pathogenesis of myocardial ischemia. Provocative test of coronary spasm during coronary arteriography is clinically useful. The ergonovine test has gained widespread use, and we have examined the efficacy and safety of intracoronary ergonovine application with a fixed dose of 16 micrograms. We studied 119 patients undergoing coronary arteriography. Coronary spasm was induced in 34 cases by intracoronary administration of 16 micrograms of ergonovine maleate. Coronary spasm was readily resolved by intracoronary administration of isosorbide dinitrate. None of the cases negative to the intracoronary ergonovine applications could be induced by additional systemic administration of 0.4 mg of ergonovine. Side effects of ergonovine such as elevation of blood pressure, headache and chest symptoms were infrequent in the intracoronary ergonovine test. We conclude that our method of intracoronary ergonovine application is sensitive and safe for the diagnosis of coronary spasm.

Aorta↗
PubMed1994

Mechanism of ergonovine-induced contraction in the mesenteric artery from deoxycorticosterone acetate-salt hypertensive rat.

Contractile responsiveness of the rat mesenteric artery to the ergot alkaloid ergonovine is enhanced in deoxycorticosterone acetate (DOCA) hypertension. This study determines if this abnormality is mediated through serotonergic or alpha adrenergic receptors and investigates the cellular mechanism of the contraction. Mesenteric arteries were dissected from DOCA hypertensive and normotensive rats for use in isolated tissue experiments. Contractions to 5-hydroxytryptamine, phenylephrine, norepinephrine, dopamine and histamine were of a similar maximum in the hypertensive and sham artery with phenylephrine, dopamine and serotonin more potent in hypertension. Ergonovine contracted hypertensive arteries (maximum = 245 +/- 27 mg) but only minimally in sham arteries (maximum = 83 +/- 19 mg). Endothelium removal did not enhance contraction to ergonovine. The alpha-1 antagonist prazosin (10(-6) M) and the serotonergic antagonist 1-naphthylpiperazine (10(-6) M) shifted the ergonovine concentration response of the hypertensive artery rightward. The alpha-2 receptor antagonist idazoxan (10(-6) M) and dopamine antagonist haloperidol did not affect contraction to ergonovine. Contraction to ergonovine was not altered by indomethacin or 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate and was minimally affected by genistein, indicating that ergonovine does not activate pathways which involve cyclooxygenase, phospholipase C or tyrosine kinases, respectively. The protein kinase C inhibitor chelerythrine (10(-5) M), nifedipine (10(-6) M) and calcium-free medium blocked ergonovine-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Mechanisms of ergonovine-induced hyperconstriction of coronary artery after x-ray irradiation in pigs.

Mechanisms of ergonovine-induced coronary hyperconstriction were examined in vivo and in vitro in miniature pigs. To provoke coronary hyperconstriction, the endothelium of a segment of a major branch of the left coronary artery was denuded in 19 Göttingen miniature pigs (4 to 6 months of age). In Group I (n = 12), the denuded site of the coronary artery was selectively irradiated with 15Gy of x-ray twice, 3 and 4 months after endothelial denudation. The remaining 7 pigs were not irradiated (Group II). The vasoconstrictive effect of intracoronary administration of ergonovine (1 to 1000 microgram) was examined angiographically 3 months (just before irradiation in group I) and 5 months after denudation in the two groups. After the angiographical study, the vessels were isolated and isometric tensions were measured in an organ chamber. In the in vivo studies, ergonovine-induced vasoconstriction at the denuded and x-ray irradiated site in Group I was significantly greater than that at the control site or that at the denuded site in Group II. Pretreatments with serotonin receptor blockers (ketanserin or methysergide) significantly attenuated ergonovine-induced hyperconstriction, while an alpha-adrenergic receptor blocker (prazosin) did not (% inhibition; ketanserin 74 +/- 9%, p < 0.01, methysergide 60 +/- 10%, p < 0.01, prazosin 9 +/- 5%, NS). In the in vitro studies, ergonovine produced significantly greater tension at the denuded and x-ray irradiated site (Group I) than at the control site or at the denuded site (Group II). Ergonovine-induced endothelium-dependent relaxation was impaired at the denuded site in both groups to a similar extent. These results suggest that ergonovine-induced hyperconstriction at the denuded and x-ray irradiated coronary artery resulted mainly from the hyperreactivity of medial smooth muscle mediated by serotonin receptors.

Animals↗
PubMedDate not supplied

Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoceptors are not involved.

The effect of i.v. ergonovine tartrate infusions (0.05-20 micrograms/kg/min, 12 minutes duration) on coronary arteries was studied in 14 conscious dogs instrumented to continuously measure vascular diameter by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Ergonovine induced a biphasic coronary response: small, transient dilation during the first minutes of infusion, followed by slowly developing constriction reaching its maximum 5 to 15 minutes after the end of the infusion and persisting at this level for at least 10 minutes. The threshold dosage for significant constriction was 0.05 microgram/kg/min. A dosage of 5 micrograms/kg/min (cumulative 60 micrograms/kg, corresponding to 35 micrograms/kg ergonovine maleate) caused a decline in mean left circumflex artery diameter by 137 +/- 15 micrometers (= 4.6%) without significantly altering heart rate, plasma catecholamines or plasma renin activity. Coronary venous O2 saturation did not decline, indicating the absence of coronary resistance vessel constriction. The epicardial artery constriction was not attenuated by a vasopressin antagonist. Under adrenergic blockade (2 mg/kg phentolamine and 2 mg/kg nadolol) or under ganglionic blockade (5 mg/kg pentolinium tartrate), ergonovine (5 micrograms/kg /min) caused substantial elevation in mean arterial pressure, while the decline in coronary artery diameter was attenuated. When this increase in arterial pressure was prevented by appropriate bleeding, the ergonovine-induced coronary constriction was not diminished by adrenergic or ganglionic blockade. The serotonin antagonist methysergide (0.5 mg/kg) completely abolished the ergonovine-induced coronary artery vasomotion. It is concluded that ergonovine in dogs causes an epicardial coronary artery constriction comparable to the diffuse coronary artery narrowing in men not suffering from variant angina pectoris. These constrictions are not mediated by an adrenergic mechanism.

Adrenergic beta-Antagonists↗
PubMed1984

Value of noninvasive assessment of patients with atypical chest pain and suspected coronary spasm using ergonovine infusion and thallium-201 scintigraphy.

Twenty-six patients with known benign coronary anatomic characteristics and atypical chest pain syndromes were evaluated for the possibility of coronary spasm. Incremental intravenous ergonovine maleate infusions were administered, and thallium-201 scintigraphy was performed at the peak dosage and during recovery in the coronary care unit. With ergonovine therapy, 4 patients (16%) had chest pain associated with electrocardiographic (ECG) or scintigraphic changes. Nine patients (35%) had chest pain without associated ECG or scintigraphic changes, and 13 patients did not have chest pain in response to ergonovine administration, although 2 (8%) had ergonovine-induced scintigraphic defects. All 4 patients with ergonovine-induced chest pain and associated ECG or scintigraphic abnormalities had resolution or reduction of chest pain after medical treatment. However, 7 of the 9 patients with ergonovine-induced chest pain in the absence of ECG or scintigraphic abnormalities continued to have symptoms despite medical treatment a mean of 18 months later. In this limited study of a select group, bedside ergonovine provocation appeared safe. Many patients had chest pain, but few showed ECG or scintigraphic evidence of ischemia. Perfusion scintigraphy appears to have potential complementary value for the identification of an ischemic cardiac cause of atypical chest pain and provides a rationale for appropriate therapy.

Adolescent↗
PubMed1999

Influence of the endothelium, nitric oxide and serotonergic receptors on coronary vasomotor responses evoked by ergonovine in conscious dogs.

1. The respective contributions of coronary vascular endothelium, nitric oxide (NO) and serotonergic receptors to the effects of ergonovine on large and small coronary arteries were investigated in conscious dogs. 2. In seven dogs with an endothelium intact, ergonovine (30 - 1000 microg, i.v.) induced a biphasic response on large coronary artery with an early and transient vasodilatation (up to +2.9+/-0.5% from 3310+/-160 microm, P<0.01) followed by a sustained vasoconstriction (down to -4.9+/-0.5%, P<0.001) which occurred simultaneously with a sustained increase in coronary blood flow (CBF) (up to +100+/-26% from 28+/-4 ml min(-1), P<0.001). After endothelium removal (balloon angioplasty), the ergonovine-induced vasodilatation was abolished and vasoconstriction potentiated (-6.4+/-0.9% after vs -4.9+/-0.5% before endothelium removal, P<0.01). 3. After blockade of NO synthesis by Nomega-nitro-L-arginine (30 mg kg(-1)) in four other dogs, the early vasodilatation induced by ergonovine was abolished but the delayed vasoconstriction as well as the increase in CBF remained unchanged. 4. Both ketanserin and methiothepin (0.3 mg kg(-1)) abolished the early vasodilatation and reduced the delayed vasoconstriction induced by ergonovine. Ketanserin decreased and methiothepin abolished the reduction in coronary resistance induced by ergonovine. 5. Thus, the complex interactions between vascular endothelium and serotonergic receptors to ergonovine-induced constriction of large coronary arteries might explain the induction of coronary spasms in patients with endothelial dysfunction.

Animals↗
PubMed1994

Once daily felodipine in preventing ergonovine-induced myocardial ischaemia in Prinzmetal's variant angina.

The efficacy of extended-release felodipine in preventing ergonovine-induced myocardial ischaemia was assessed in 14 patients (12 male, two female, aged 56 +/- 7 years) with Prinzmetal's variant angina. Four of the patients had normal coronary arteries, eight had one-vessel and two had two-vessel disease. The ergonovine test was performed once in basal conditions and twice 5 days after beginning the oral administration of felodipine 20 mg o.d., 4 and 24 h after the last administration. During a continuous 6-lead ECG recording, ergonovine was injected at doses of 25, 50, 100, 200, and 400 micrograms at 5 min intervals. Blood samples for felodipine plasma concentrations were drawn at the time of the tests. The basal ergonovine test was positive in all 14 patients (seven with anterior and seven with inferior ST segment elevation > 0.1 mV) at a mean ergonovine dose of 162 +/- 138 micrograms. The test was repeated 4 h after the last felodipine administration and was negative in 13 patients (93%), but 24 h after the last drug administration, eight patients (57%) had a positive test response (five with anterior, three with inferior ST segment elevation) at a higher ergonovine dose than at baseline (150 vs 97 micrograms, P = 0.042). The only differences between patients with a negative and a positive test were the mean values of the left ventricular end-diastolic pressure (9.3 vs 14.9 mmHg, P = 0.002) and the ergonovine doses used in the baseline tests (250 vs 97 micrograms, P = 0.034).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1979

Similarities of ergonovine-induced and spontaneous attacks of variant angina.

Ergonovine has been shown to provoke attacks of variant angina, but a question remains whether spontaneous and ergonovine-induced attacks of variant angina are similar. Seven patients with variant angina undergoing cardiac catheterization were studied during transient episodes of spontaneous and ergonovine-induced rest angina with ST-segment elevation. Clinical, electrocardiographic, left ventricular hemodynamic and coronary angiographic observations were made before and repeated after ergonovine (0.05-0.2 mg I.V.). The character and duration of chest pain were similar during both spontaneous and ergonovine-induced episodes. ST-segment elevation (greater than 1 mm) was present inferiorly in three patients, anteriorly in three patients, and both inferiorly and anteriorly in one patient during both episodes. Mean heart rate and systolic arterial pressure changed little, while left ventricular end-diastolic pressure increased significantly during spontaneous or ergonovine-induced attacks. We observed subtotal or total dynamic obstruction in the left anterior descending (three patients), right coronary arteries (three patients) and both arteries in one patient during both attacks. Thus, in selected patients ergonovine-induced attacks of variant angina were remarkably similar to spontaneous episodes.

Adult↗
PubMed1983

Comparative sensitivity of exercise, cold pressor and ergonovine testing in provoking attacks of variant angina in patients with active disease.

Exercise, ergonovine and the cold pressor test have been used to provoke variant angina attacks. The sensitivity of these three tests was compared in 34 hospitalized patients with well documented, active variant angina who had recently undergone coronary arteriography. The three tests were usually performed on three consecutive days, and 28 of the 34 had the three tests within 1 week. Angina was provoked by ergonovine in all 34 patients, by exercise in 17 and by cold pressor test in only five (p less than 0.005). ST elevation developed during the ergonovine test in 32 (94%), during exercise in 10 (29%) and during the cold pressor test in only three (9%). With ergonovine, one patient had only ST depression and one had no ECG changes. During the cold pressor test two patients had pseudonormalization of abnormally negative T waves and 29 had no ECG changes. Exercise induced T-wave pseudonormalization in four patients, ST depression in nine others and no ECG changes in 11. ST elevation was more frequent with ergonovine than with either of the other tests (p less than 0.0001). ST elevation or T-wave pseudonormalization occurred more often with exercise than with cold (p less than 0.05), but both occurred less often than with ergonovine (p less than 0.0001). We conclude that the sensitivity of the ergonovine test is very high in patients with active variant angina and that exercise will provoke angina with ST elevation in about 30% of these cases. In contrast, the sensitivity of the cold pressor test is too low to be of much clinical value in the diagnosis of variant angina.

Adult↗
PubMed1992

Mechanism of ergonovine-induced hyperconstriction of the large epicardial coronary artery in conscious dogs a month after arterial injury.

This study investigated the mechanism of ergonovine-induced hyperconstriction of coronary artery in conscious dogs that had undergone endothelial denudation one month earlier. The diameter of the large epicardial coronary artery was continuously measured by a sonomicrometer in 12 dogs in which two pairs of 10-MHz piezoelectric crystals had been surgically implanted at the denuded and nondenuded sites of coronary arteries. A month after the endothelial denudation, intravenous ergonovine (0.01, 0.1, 0.3, and 1.0 mg) produced transient dilation followed by dose-dependent constriction. The degrees of dilation were comparable between the denuded and nondenuded sites. The magnitudes of constriction induced by ergonovine were significantly larger in the denuded site than in the nondenuded site: the percent reductions in diameter evoked with 0.3 mg ergonovine were 14.4 +/- 2.3% and 3.8 +/- 0.8% (p less than 0.01) at the denuded and nondenuded sites, respectively. The magnitudes of constriction induced by intravenous phenylephrine (0.02, 0.06, and 0.2 mg) were comparable in the denuded and nondenuded sites. Methysergide (a nonselective serotonergic blocker) in a dose of 0.5 mg/kg significantly inhibited vasoconstriction induced by ergonovine (0.3 mg) from 13.1 +/- 1.1% to 2.7 +/- 1.0% (p less than 0.01) at the denuded site and from 4.2 +/- 0.6% to 0.8 +/- 0.3% (p less than 0.05) at the nondenuded site. Diltiazem (1.0 mg/kg) selectively inhibited the ergonovine-induced hyperconstriction. Ketanserin (0.5 mg/kg), prazosin (1.0 mg/kg), or indomethacin (5.0 mg/kg) did not prevent the ergonovine-induced hyperconstriction. Histological study revealed intimal thickening and regenerated endothelium in the denuded site.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Increased numbers of sperm in the oviducts and improved fertilization rates in rabbits after administration of phenylephrine or ergonovine near the time of insemination.

Phenylephrine, an alpha-adrenoceptor agonist, was administered im to does near the time of mating or insemination. The treatment increased sperm numbers in the oviducts by about 50-fold and in the uterus by about 10-fold at 2 or 2.5 h after insemination. Methoxamine, another alpha-adrenoceptor agonist that was given im, did not increase sperm numbers, although both phenylephrine' and methoxamine significantly increased the number and amplitude of uterine contractions when contractions were measured by strain gauge force transducers attached to the uterus of conscious does. Ergonovine, an ergot derivative given im, increased sperm numbers more than 10-fold in the oviducts and five to 10-fold in the uterus at 2 or 2.5 h after insemination. Ergonovine increased the frequency and amplitude of uterine contractions when given iv but not when given im. In tests with a range of doses of phenylephrine and ergonovine, 5 mg of phenylephrine and .6 mg of ergonovine appeared to be near optimal for maximizing the number of sperm in the uterus and oviducts at 2.5 h after insemination. Phenoxybenzamine, an alpha-adrenoceptor blocking agent, prevented the phenylephrine-induced increases in both uterine contractions and sperm numbers in the oviducts and uterus. Phenoxybenzamine also prevented the effect of ergonovine on sperm numbers. In does inseminated with low numbers of sperm (92,000; an inseminate selected to result in a low fertilization rate in control does), the administration of phenylephrine or ergonovine significantly increased ovum fertilization rates (16% for control does, 52 and 63%, respectively, for phenylephrine- and ergonovine-treated does).

Animals↗
PubMed1984

Improvement by ergonovine of sperm transport, fertilization and pregnancy rates in ewes in natural or prostaglandin-induced estrus.

Eight experiments were conducted with 451 ewes to test effects of ergonovine, prostaglandin F2 alpha (PGF2 alpha) and phenylephrine on sperm transport and fertility. In most experiments, ewes were mated at estrus and necropsied 2 or 3 h later. Sperm were flushed from the oviducts, uterus and anterior, middle and posterior thirds of the cervix and counted. Various doses of PGF2 alpha or phenylephrine given im at mating caused no significant increase in sperm numbers in any segment of the tract 2 h later. Three different dose levels of ergonovine were given im to ewes in natural estrus 1 h after mating and ewes were necropsied 3 h after mating. Doses of .2 and 1.0 mg were ineffective, but .5 mg increased sperm numbers about 10-fold in the oviducts and uterus. When given im at the time of artificial insemination, .6 mg of ergonovine increased the fertilization rate at 3 d from 5/25 in control ewes to 12/25 (P less than .05). In three experiments with ewes in PGF2 alpha-induced estrus, .6 mg of ergonovine increased sperm numbers in the cervix and uterus at 3 h after mating and in the uterus and oviducts at 23 h, near ovulation. Other ewes were artificially inseminated in the external cervical os and one-half of the ewes were given .6 mg of ergonovine im; ewes not returning to estrus were laparotomized at 22 to 26 d and embryos removed. After insemination during natural estrus with .2 ml of semen, pregnancy rates were 14/25 for control ewes and 15/25 for ergonovine-treated ewes; after insemination during natural estrus with .1 ml of semen, 6/35 and 18/35 (P less than .005); after insemination during PGF2 alpha-induced estrus with .2 ml of semen, 7/60 and 12/60. Fertilization and pregnancy rates combined were 32/145 (22%) for all control ewes and 57/145 (39%) for ergonovine-treated ewes (P less than .005).

Animals↗
PubMed1983

Assessment of sublingual isosorbide dinitrate and intracoronary nifedipine during ergonovine provocation.

In 37 patients with suspected vasospastic angina diagnostic ergonovine testing was used as a method of analysing the efficacy of sublingual ISDN in comparison with sublingual and intracoronary nifedipine on coronary luminal diameter, left ventricular ejection fraction, aortic blood pressure, heart rate and left ventricular end-diastolic pressure. 10 mg of sublingual ISDN counteracted the ergonovine effects on left ventricular pump function and hemodynamics. The luminal diameter of the epicardial coronary arteries increased from 3.5 +/- 0.8 to 4.9 +/- 0.8 mm. 20 mg of sublingual nifedipine did not change the coronary luminal diameter within 8-10 minutes after the ergonovine test. After administration of 0.1 mg of nifedipine into the right and left coronary artery the luminal diameters increased in the same range as after sublingual ISDN. Whereas the aortic blood pressure decreased after intracoronary nifedipine from 170 +/- 23 to 153 +/- 27 mmHg with a concomitant increase in heart rate, no effect on the left ventricular pump function could be assessed. In the model of ergonovine testing ISDN has shown itself as a potent drug in releasing the ergonovine effects. Sublingual ISDN is as potent as intracoronary nifedipine in releasing the ergonovine-induced reduction of coronary luminal diameters and more potent in counteracting the ergonovine effects concerning the cardiac pump function.

Adult↗
PubMed1990

Intravenous nifedipine prevents ergonovine-induced myocardial ischemia in patients with stable effort angina.

Twelve of 40 consecutive patients with effort angina, documented coronary artery disease, and a positive exercise stress test had a positive ergonovine test. ST-segment depression (0.1 mV) occurred in ten and ST elevation (0.1 mV) in two patients. During the ergonovine maleate test the rate-pressure product recorded at the onset of ischemia (ST greater than or equal to 0.1 mV) was significantly lower than that recorded during the exercise stress test. The reproducibility of the rate-pressure product at ischemia was displayed in every patient with a second test; then, a third test after intravenous nifedipine infusion (1 mg over 5 minutes + 1 mg over 55 minutes) was performed. Six patients had negative results; out of the remaining six, three exhibited a significant increase in the dosage required for provoking ischemia. Both systolic and diastolic blood pressure were reduced by nifedipine, while only a slight increase in heart rate occurred, so that the rate-pressure product at any ergonovine dosage was decreased by nifedipine. No differences in the ischemic threshold during exercise and during the ergonovine maleate tests (in washout and after nifedipine) were found in patients with a positive or negative response to nifedipine. The ergonovine test was positive in a sizable (30%) number of patients with stable effort angina. In these patients nifedipine was effective in preventing ergonovine-induced myocardial ischemia.

Angina Pectoris↗