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)

A possible effectiveness of atropine on variant form of angina pectoris was investigated using the left circumflex coronary arterial strips of dogs. Acetylcholine 10(-5)--10(-3) Gm/ml dose-dependently constricted the isolated arterial strips during potassium-contracture in 6 cases, and repetitive applications of acetylcholine could produce the similar contractions to the control. In 18 strips atropine 10(-6) Gm/ml significantly depressed the contractions of coronary arteries induced by acetylcholine 10(-5)--10(-3) Gm/ml. In 5 arterial strips atropine 10(-6) Gm/ml significantly inhibited norepinephrine-induced responses of these arteries, and by 10(-5) Gm/ml further suppression of the responses was obtained. The results suggest that atropine may suppress the contractile responses of the coronary artery induce by acetylcholine and nonrepinephrine through a muscarinic-receptor blocking action and simultaneously partly through an adrenergic alpha-receptor blocking action.
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PMID:Inhibition of constrictor responses of dog coronary artery by atropine. A possible effectiveness of atropine on variant form of angina pectoris. 44 44

In order to evaluate the effects of intracoronary acetylcholine on coronary resistance vessels, oxygen saturation in coronary sinus blood was continuously measured to compare its dynamic changes during intracoronary injection of acetylcholine in both patients with variant angina and control subjects. Group 1 consisted of 6 patients without coronary artery disease. Group 2 consisted of 10 patients with variant angina and spasm in the left anterior descending coronary artery. A fiberoptic reflection oximetry system was used for the continuous measurement of coronary sinus venous oxygen saturation. Acetylcholine (20 micrograms) was injected directly into the left coronary artery over 30 s. In the group 1 patients, coronary sinus venous oxygen saturation was increased from 39 +/- 2% (mean +/- SEM) to 54 +/- 3% at 30 s, continuously climbed to 70 +/- 3% at 60 s and then gradually decreased to 53 +/- 5% at 120 s after the initiation of intracoronary injection of acetylcholine. In contrast, in the group 2 patients, coronary sinus venous oxygen saturation was transiently increased from 39 +/- 2% to 56 +/- 4% at 30 s, reversed, decreased to 52 +/- 4% at 60 s and then rapidly decreased to 36 +/- 3% at 120 s with the onset of chest pain associated with electrocardiographic ischemic changes. Coronary arteriography during attacks demonstrated a total or subtotal occlusion of the left anterior descending coronary artery due to severe spasm in all of the 10 patients. The extent of increases in coronary sinus venous oxygen saturation at 30 s after acetylcholine injection was not significantly different between the two groups (group 1: 15 +/- 4%, group 2: 17 +/- 3%). Heart rate, blood pressure and rate-pressure product were essentially unchanged at 30 s after intracoronary injection of acetylcholine in both groups. These data suggest that in control adult humans, coronary blood flow was increased through dilatation of resistance vessels by acetylcholine, while in patients with variant angina, coronary blood flow was transiently increased by dilatation of resistance vessels, after which it was suddenly decreased by spasm of an epicardial artery induced by this agent. Relaxant responses to acetylcholine of coronary resistance vessels appear to be preserved well in patients with variant angina.
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PMID:Biphasic changes (initial increase and late decrease) in coronary sinus venous oxygen saturation during anginal attacks induced by intracoronary acetylcholine in patients with variant angina. 130 Dec 47

To examine the constrictor response of the infarct-related stenotic coronary artery in comparison with that of noninfarct-related stenotic arteries, acetylcholine in maximal doses of 100 micrograms for the left and 50 micrograms for the right coronary artery was injected into the 16 infarct-related coronary arteries of 16 patients with previous myocardial infarction (group 1) and into 19 stenotic coronary arteries of 16 patients with stable angina without myocardial infarction (group 2). Acetylcholine's effects on lumen diameter and area were quantitatively analyzed at the stenotic segment and its proximal segment without significant stenosis. Acetylcholine decreased lumen diameter and area at the stenotic segments from 0.72 +/- 0.18 to 0.18 +/- 0.33 mm and from 0.45 +/- 0.22 to 0.10 +/- 0.22 mm2, respectively, in group 1 (both p less than 0.01) and from 0.75 +/- 0.22 to 0.49 +/- 0.30 mm and 0.48 +/- 0.29 to 0.26 +/- 0.23 mm2, respectively, in group 2 (both p less than 0.01). Acetylcholine decreased the diameter and area at the proximal segment from 2.71 +/- 0.75 to 2.38 +/- 0.6 mm and from 6.18 +/- 3.4 to 4.71 +/- 2.23 mm2, respectively, in group 1 (both p less than 0.01) and from 2.31 +/- 0.67 to 1.95 +/- 0.59 mm and from 4.5 +/- 2.97 to 3.22 +/- 1.96 mm2, respectively, in group 2 (both p less than 0.01). The changes in diameter and area at the stenotic segment in group 1 were significantly greater than those in group 2 (both p less than 0.01); there were no significant differences between groups in the changes at the proximal segment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of acetylcholine on the highly stenotic coronary artery: difference between the constrictor response of the infarct-related coronary artery and that of the noninfarct-related artery. 154 69

The epicardial coronary artery of patients with variant angina is hyperreactive to the constrictive effect of acetylcholine, but it is not known whether the coronary microvasculature also constricts in response to acetylcholine. Incremental doses of acetylcholine were injected into the left coronary artery of 57 patients with variant angina and with spasm in this artery. By measuring coronary sinus blood flow, coronary hemodynamic status just before angiographic documentation of spasm was examined. Acetylcholine induced spasm in the left coronary artery in all patients. It also decreased the diameter of the nonspasm artery by 36 +/- 19% from baseline. For all patients, coronary sinus blood flow was 89 +/- 38 ml/min at baseline and increased to 104 +/- 61 ml/min during an acetylcholine-induced anginal attack (p less than 0.01). In 10 patients with spasm in both the left anterior descending and left circumflex arteries (that is, multivessel spasm), coronary sinus blood flow decreased from 84 +/- 21 to 52 +/- 26 ml/min (p less than 0.01). In the other 47 patients with spasm in only one of these two arteries (that is, single-vessel spasm), coronary sinus blood flow increased from 90 +/- 41 to 115 +/- 61 ml/min (p less than 0.01) without change in the rate-pressure product. It is concluded that in patients with variant angina, acetylcholine induces spasm and constriction in the epicardial coronary artery, whereas it dilates the resistance vessels presumably through the release of the endothelium-dependent relaxing factor.
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PMID:A study on coronary hemodynamics during acetylcholine-induced coronary spasm in patients with variant angina: endothelium-dependent dilation in the resistance vessels. 159 35

Acetylcholine-induced constriction of human coronary arteries in vivo is commonly attributed to endothelial dysfunction. To examine the effects of 2 other important determinants of vascular responses--namely, agonist concentration and the segment of circulation under study--the diameters of proximal, middle and distal segments of the left anterior descending artery (LAD) and coronary sinus oxygen saturation were measured in 10 patients with angiographically normal coronary arteries (group 1) and in 7 patients with coronary atherosclerosis (group 2) after intracoronary acetylcholine was infused at concentrations from 10(-7)M to between 10(-4)M and 10(-2)M. In group 1, acetylcholine caused minor (less than or equal to 6%) but progressive dilatation of the LAD up to 10(-4)M, but constriction, particularly of the distal segments and tertiary branches, occurred at higher concentrations. Over the same concentration range, coronary sinus oxygen saturation rose progressively from a basal level of 36 +/- 3% to a maximum of 72 +/- 3% in the absence of changes in heart rate and blood pressure, suggesting marked progressive dilatation of resistance vessels. Concentrations greater than or equal to 10(-3)M caused intense constriction of distal epicardial vessels and, in some cases, anginal pain and objective signs of ischemia. Conversely, in group 2, acetylcholine (infused only up to 10(-4)M for ethical reasons) failed to cause significant changes in LAD diameter. These data suggest that the local acetylcholine concentration and coronary vascular segment under study may determine the observed response to at least an equivalent extent as does the presence or absence of coronary atherosclerosis, raising the question of whether a constrictor response to intracoronary acetylcholine reliably indicates the presence of coronary atherosclerosis.
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PMID:Response of angiographically normal and atherosclerotic left anterior descending coronary arteries to acetylcholine. 222 Jun 34

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Induction of coronary arterial spasm by intracoronary administration of acetylcholine in patients with vasospastic angina]. 264 69

Acetylcholine (20 to 100 micrograms) was infused directly into coronary arteries in 10 patients with variant angina (group A), 13 subjects without coronary artery disease (group B) and 8 patients with significant organic coronary artery stenosis (greater than or equal to 50%) but without variant angina (group C) during coronary arteriography, to clarify the action of this agent on coronary arteries. Temporary pacing was performed at a demand heart rate of 40 beats/min while bradyarrhythmia developed. Coronary arteriography after administration of acetylcholine showed coronary vasoconstriction in all 10 patients (100%) of group A. Angina accompanied by electrocardiographic ischemic changes in 9 of 10 (90%, 7 ST-segment elevation and 2 depression) was provoked during this test. In the patients of group B, acetylcholine also induced vasoconstriction in 8 of 22 (36%) coronary arterial systems examined, chest pain in 3 (14%) and ST-segment deviation in none (0%). In the patients of group C, acetylcholine induced vasoconstriction in 3 of 9 (33%), chest pain in 2 (22%) and ST-segment depression in 1 (11%). No definite coronary artery dilation induced by acetylcholine was noted. Coronary vasoconstriction (p less than 0.05), electrocardiographic ischemic findings (p less than 0.01) and chest pain (p less than 0.01) were induced significantly more frequently in group A than in both groups B and group C. No significant difference was found between group B and group C. The coronary arteries in the patients with variant angina seem to be more susceptible to acetylcholine than those of patients without variant angina irrespective of the presence of significant atherosclerosis.
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PMID:Supersensitivity of coronary arteries in variant angina to spasm induced by intracoronary acetylcholine. 333 20

This study examined the question of whether intracoronary administration of nitroglycerin modifies contralateral intracoronary acetylcholine test results. Acetylcholine was injected separately into both left and right coronary arteries in 63 patients with coronary spastic angina. Acetylcholine (20 and 50 micrograms) was injected first into the coronary artery responsible for the documented regional ischemia during spontaneous or induced attacks, and then into the other coronary artery. Coronary spasm was defined as severe transient coronary artery vasoconstriction with chest pain and/or electrocardiographic ischemic ST-segment deviation. Spasm was induced in either coronary artery in 60 patients (95%) and in both coronary arteries in 23 patients (37%). The frequency of induced spasm was 67% (42 of 63) in the coronary artery first challenged by acetylcholine. The coronary artery spasm subsided with the intracoronary injection of nitroglycerin (250-750 micrograms) in 19 patients. In the second challenge of intracoronary acetylcholine injection into the contralateral coronary artery, coronary spasm was induced in 29 (66%) of 44 patients. This was done without intracoronary administration of nitroglycerin in the first challenge and in 12 (63%) of 19 patients who had been given intracoronary nitroglycerin. The sensitivity for spasm induced by intracoronary acetylcholine appeared to be unaffected by nitroglycerin. Coronary spasm with ST-segment elevation by intracoronary acetylcholine in the second challenge was significantly less frequent in the patients receiving intracoronary acetylcholine in the second challenge was significantly less frequent in the patients receiving intracoronary nitroglycerin (first: 89%, second: 26%, p < 0.05) as well as in those not receiving intracoronary nitroglycerin for the spasm in the first challenge (first: 52%, second: 13%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intracoronary administration of nitroglycerin on contralateral intracoronary acetylcholine test results. 844 91

This study investigated whether the maximal dose of 50 micrograms acetylcholine for the induction of coronary spasm in the right coronary artery is adequate. The acetylcholine test was performed in 388 consecutive patients to evaluate spasm from January 1994 to December 1997. Coronary spasm in the right coronary artery was induced in 43 patients, 37 men and 6 women with a mean age of 63 +/- 8 years by intracoronary injection of 80 micrograms of acetylcholine rather than 50 micrograms. These included 15 patients (35%) with rest angina, 23 patients with ischemic heart disease other than rest angina and 5 patients (12%) with non-ischemic heart disease. Acetylcholine was injected in incremental doses of 20, 50 and 80 micrograms into the right coronary artery. Positive spasm was defined as induction of more than 90% reversible narrowing associated with either usual chest pain or ischemic electrocardiographic changes. Clinical and angiographical characteristics was studied in these patients. Fifteen (35%) patients had rest angina and 4 patients had variant angina with ST elevation in the inferior leads. Two thirds of the patients had coronary spasm in the distal portion of the right coronary artery and one third of those disclosed spasm focally. Coronary spasm was induced in 38 (15%) of 246 patients with ischemic heart disease and in 5 (4%) of 142 patients with non-ischemic heart disease. The prevalence of positive spasm in patients with ischemic heart disease was significantly higher (p < 0.01) than in patients with non-ischemic heart disease. A dose of 80 micrograms of acetylcholine, more than the maximal standard dose, might be clinically useful for the induction of spasm in the right coronary artery if coronary spasm of this artery is strongly suspected.
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PMID:[Absence of induced spasm by intracoronary injection of 50 micrograms acetylcholine in the right coronary artery: usefulness of 80 micrograms of acetylcholine as a spasm provocation test]. 978 36

This study examined the direct response of smooth muscle of coronary spasm sites to alpha1-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 microM in the coronary circulation, for 5 min), a stimulator of alpha1-adrenoreceptors, was directly infused into coronary arteries with spasm in 10 patients with coronary spastic angina and into normal coronary arteries in 10 control patients. The luminal diameter of epicardial coronary arteries was determined by computer-assisted quantitative angiography. The constrictor response to intracoronary injection of acetylcholine (ACh; 50 microg) was greater in spastic arteries than in control arteries (decrease from baseline, 48+/-2% vs. 12+/-2%, respectively; p<0.001). ACh (50 or 100 microg) induced coronary spasm associated with myocardial ischemia in all of patients with coronary spastic angina but not in any control patients. On the other hand, phenylephrine infusion did not induce coronary spasm in any of patients with coronary spastic angina or in control subjects. The constrictor response to phenylephrine infusion was comparable between spasm and control coronary arteries (decrease from baseline, 11+/-2% vs. 9+/-2%, respectively; p = NS). The results indicate that smooth muscle of spastic coronary arteries does not exhibit enhancement of constrictor response to direct stimulation of alpha1-adrenoreceptor on coronary smooth muscle. There may be receptor-specific enhancement of constrictor response to agonists in smooth muscle of spastic coronary arteries in patients with coronary spastic angina.
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PMID:Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina. 1006 77


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