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)

To assess possible coronary vasoconstriction in patients with ischemic heart disease, we measured coronary vascular resistance in 12 patients with normal hearts and 12 with coronary disease before and during the initial 50 seconds of cold pressor test, a stimulus known to produce systemic vasoconstriction. Control coronary vascular resistance was similar in the two groups, and although it did not change in patients with normal vessels, it rose by 27 per cent (P less than 0.005) in the group with coronary disease during the cold pressor test. In three of 12 patients with coronary disease coronary flow actually declined despite an increase in arterial pressure; in four, angina was precipitated. Phentolamine abolished increases in arterial pressure and coronary vascular resistance during the test in three patients with coronary disease. Adrenergically mediated coronary vascular tone may be an important determinant of coronary blood flow and may contribute to ischemia in patients with coronary disease.
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PMID:Reflex increase in coronary vascular resistance in patients with ischemic heart disease. 1 May 27

The clinical uses of phentolamine have widened since its introduction as an anti-hypertensive agent. The vasodilating action of the drug as well as its postive inotropic effects have led to its use in treating congestive heart failure. Recently, phentolamine has been use by several groups to improve left ventricular function in acute myocardial infarction. There appears to be great promise for the use of phentolamine in this clinical setting. The drug given intravenously or orally can suppress ventricular premature beats and supraventricular premature beats. However, the experience of phentolamine as an antiarrhythmic agent is still limited. Similarly, the relief of angina pectoris by phentolamine requires confirmation by additional clinical studies. Phentolamine can be used as a provocative test in idiopathic hypertrophic subaortic stenosis. Since it does not produce cardiac arrhythmias, it may be safer than isoproterenol. The comparative effectiveness of phentolamine and isoproterenol in diagnosing I.H.S.S. is unknown. Phentolamine has been advocated for several years as a beneficial agent for the treatment of shock. The experience is still limited to a few groups who have reported favorable results. Phentolamine has been used as a bronchodilator and a pulmonary artery dilator. The preliminary reports appear favorable. However, continused investigation is warranted. A sensitive measurement of the blood levels of phentolamine is not available. When this is accomplished, further insight into the metabolism of this drug will be forthcoming.
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PMID:Phentolamine. 94 32

Propranolol is a commonly used drug; of new and refilled prescriptions, it ranked no. 1 in 1984 and no. 2 in 1985. Medical conditions for its use include angina pectoris, myocardial infarction, hypertension, cardiac dysrhythmias, hypertrophic subaortic stenosis, migraine headache, hyperthyroidism, and pheochromocytoma. Almost all dental practitioners will treat a patient receiving propranolol for one of these conditions. The following recommendations seem appropriate at this time: The patient should continue to receive propranolol during dental treatment. Sudden withdrawal of the beta-blocker will cost the patient the benefit of propranolol therapy and may lead to acute myocardial ischemia. Acute stress should be minimized, as hypertensive responses may also be caused by endogenously released epinephrine. Short appointments scheduled in the morning, possibly with conscious sedation, should be considered. The dosage of adrenergic vasoconstrictors should be limited and gingival retraction cord containing epinephrine avoided entirely. The blood pressure should be taken approximately 5 minutes after local anesthesia is administered to determine if a systemic response has occurred. In the unlikely event of a hypertensive emergency, a rapidly acting, short-duration antihypertensive drug, such as the alpha-blocker phentolamine (Regitine, 5 mg intravenously) should be administered. Sublingual nitroglycerin (Nitrostat, 0.4 mg) may be useful as a nonparenteral alternative. These recommendations apply to other nonselective beta-blockers, including nadolol (Corgard) and timolol (Blocadren). They may also apply to labetalol (Normodyne, Trandate), a nonselective beta-antagonist with some alpha-blocking activity and to pindolol (Visken), a beta-blocker with some intrinsic beta 2-agonistic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive response to levonordefrin in a patient receiving propranolol: report of case. 327 28

Ethanol produces in vitro vasoconstriction of coronary arteries and can precipitate angina in patients with coronary obstructive disease. To demonstrate the in vivo effect of ethanol on coronary dynamics, baseline measurements of left anterior descending (LAD) coronary artery dimension by quantitative angiography, hemodynamics, arterial and coronary sinus blood gases, and blood ethanol levels were obtained in 14 closed-chest mongrel dogs. Three ethanol levels were established by intravenous bolus followed by 1-hour maintenance infusions. All measurements made at baseline were recorded every 30 minutes. Phentolamine (5 mg i.v.) and nicardipine (0.15 mg/kg i.v.) were given to evaluate constrictor mechanisms. Blood ethanol levels achieved at 60, 120, and 180 minutes were 649 +/- 48, 1,285 +/- 81, and 2,546 +/- 130 micrograms/ml, respectively. LAD cross-sectional area was reduced significantly from control at the end of each of the three dosing periods (-24 +/- 5%, -40 +/- 3%, and -53 +/- 3%; p less than 0.004). alpha-Adrenergic blockade had no effect on LAD cross-sectional area, while nicardipine partially reversed the ethanol-induced vasoconstriction. No significant change in vessel cross-sectional area took place in control dogs. These data suggest that ethanol induces epicardial coronary artery vasoconstriction in dogs at clinically important blood levels. alpha-Adrenergic blockade does not alter or reverse ethanol-induced vasoconstriction, while calcium channel blockade appears to be an effective vasodilator of ethanol-constricted vessels.
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PMID:Ethanol causes epicardial coronary artery vasoconstriction in the intact dog. 338 1

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.
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PMID:Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review. 633 4

Vasomax is an oral preparation of phentolamine mesilate (Zonagen Pharmaceuticals) currently undergoing worldwide regulatory approval for distribution. Phentolamine is primarily an alpha-adrenergic antagonist with mild sympatholytic action and a beta-adrenergic stimulating action. Over 30 years of clinical experience has shown it to be a strong direct vasodilator on muscular walled vessels, likely based on its inhibitory action on adenosine 5-triphosphate-sensitive potassium channels. This medication is not new, having been marketed in the United States in an oral formulation between 1952 and 1984. Phentolamine initially achieved FDA approval for preoperative use in patients with pheochromocytoma for control of blood pressure and paroxysmal hypertensive episodes. In the past it had been evaluated for hypertension, pulmonary disease, cardiac arrhythmias, angina pectoris and peripheral vascular disease. Unfortunately for most of these indications the clinical responses to oral phentolamine have been variable. The most clinically significant adverse events associated with oral phentolamine in the past were systemic hypotension and vasomotor collapse, severe gastrointestinal side effects especially diarrhea and some complaints of nasal congestion. In this review we will concentrate on phentolamine in a new preparation for on demand treatment of erectile dysfunction of mild to moderate degrees.
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PMID:Oral phentolamine (Vasomax). 1287 9