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)

Labetalol (Trandate; Allen & Hanbury) was administered to 17 hypertensive patients with angina pectoris, which had persisted despite blood pressure control on treatment including beta-blocking agents. In comparison with placebo, labetalol significantly reduced the frequency and severity of attacks of angina pectoris, without further improvement in control of blood pressure at rest, during isotonic exercise or on performance of the cold pressor test. Labetalol significantly reduced blood pressure levels during isometric exercise but did not reduce the systolic pressure- heart rate product. Labetalol improved the angina without evidence of causing a reduction of cardiac work (and presumably oxygen consumption by the myocardium) in comparison with the other antihypertensive agents used in this study. A possible mechanism whereby labetalol increases myocardial blood supply in hypertensive patients with angina pectoris is by an increase in coronary perfusion due to its vasodilator action.
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PMID:Beneficial effect of labetalol in hypertensive patients with angina pectoris. 684 67

Labetalol, an alpha and beta receptor blocking agent, was evaluated in 11 patients with documented coronary artery disease and stable angina. The mean dose of labetalol was 1.5 (range 1 to 2) mg/kg. Cardiovascular effects began within 1 minute after injection and were maximal within 10 minutes. Mean arterial pressure decreased from 105 +/- 13 to 81 +/- 10 mm Hg (p less than 0.0001), heart rate from 70 +/- 10 to 66 +/- 7 beats/min (p less than 0.05) and the pressure-rate product from 10,322 +/- 2,344 to 7,171 +/- 1,650 (p less than 0.001). Cardiac output and pulmonary wedge pressure did not change significantly. Mean pulmonary arterial pressure decreased from 20 +/- 3 to 16 +/- 2 mm Hg (p less than 0.005). Systemic and pulmonary resistances also decreased significantly (p less than 0.0001 and p less than 0.01, respectively). Coronary sinus flow increased from 107 +/- 26 to 118 +/- 25 ml/min (p less than 0.01) and coronary vascular resistance decreased from 1.0 +/- 0.2 to 0.77 +/- 0.1 mm Hg/ml per min (p less than 0.001). Labetalol may be a useful adjunct in the treatment of angina not only because it diminishes myocardial oxygen requirements but also because it improves coronary hemodynamics. Thus, labetalol appears to have some advantage compared with the usual beta blocking agents with their potentially detrimental effects on coronary hemodynamics.
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PMID:Hemodynamic and coronary effects of intravenous labetalol in coronary artery disease. 706 51

The immediate haemodynamic dose response effects of beta blockade (propranolol: 2 to 16 mg) were compared with those of combined alpha beta blockade (labetalol: 10 to 80 mg) in a randomised study of 20 patients with stable angina pectoris. After control measurements, the circulatory changes induced by four logarithmically cumulative intravenous boluses of each drug in equivalent beta blocking doses were evaluated at rest, after which comparison of the effects of the maximum cumulative dose of each was undertaken during a four minute period of supine bicycle exercise. Propranolol, at rest, induced significant dose related reductions in heart rate and cardiac output, with reciprocal increases in the systemic vascular resistance and pulmonary artery occluded pressure; systemic arterial pressure was unchanged. Labetalol was followed by significant dose related decreases in systemic blood pressure and vascular resistance associated with a significant increase in cardiac output; heart rate and pulmonary artery occluded pressure were unchanged. The slope of the left ventricular pumping function curve relating output to filling pressure from rest to exercise was significantly depressed by propranolol but unchanged after labetalol. The less deleterious effects on left ventricular haemodynamic performance after alpha beta blockade in contrast to beta blockade alone in ischaemic heart disease may be attributable to the concomitant reduction in left ventricular afterload associated with the alpha blocking activity of labetalol.
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PMID:Comparative haemodynamic dose response effects of propranolol and labetalol in coronary heart disease. 712 88

beta-adrenoceptor-blocking drugs, first introduced for the treatment of symptomatic angina pectoris, have been found effective across the whole spectrum of ischaemic disease. Labetalol was the first combined-action beta-blocking drug to be described and was shown to be capable of increasing exercise tolerance in patients with angina pectoris. Carvedilol also possesses a peripheral vasodilating action mainly due to an alpha 1-adrenoceptor blockade. Haemodynamic studies with carvedilol in patients with ischaemic heart disease have shown a reduction in peripheral vascular resistance in contrast to propranolol which increases systemic resistance and reduces cardiac output. Additionally, in ischaemic heart failure there is evidence of improved myocardial function, as shown by an increase in ejection fraction, after the administration of carvedilol. Carvedilol has been shown to improve exercise tolerance in patients with angina pectoris and reduce the occurrence of episodes of silent myocardial ischaemia. Carvedilol, unlike many beta-blocking drugs, does not adversely affect the plasma lipid profile qualitatively or quantitatively. In contrast to many non-selective beta-blocking drugs, carvedilol has a more favourable haemodynamic profile, and its lack of adverse influence on the plasma lipid profile may be important in its long-term use.
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PMID:Carvedilol in ischaemic heart disease. 810 63

Although their specific mechanisms of action are incompletely understood, beta blockers are most likely lower blood pressure and provide target organ protection by several different mechanisms, including inhibition of renin-angiotensine system by decreasing renin release by the jugstaglomerular cells of the kidney, central inhibition of sympathetic nervous system outflow and slowing of heart rate with a decrease in cardiac output. These agents are widely recommended as important parts of antihypertensive regimens and as well as preferred therapies for patients at high risks of coronary heart disease, and including those with angina pectoris, myocardial infarction or heart failure. The third generation beta blockers are distinguished from the earlier class of beta blockers by their vasodilating activity. Labetalol, carvedilol and bucindolol appear to provide a vasodilation primarily through their blockade of alpha-1 rerceptors. Nebivolol is a lipophilic beta reseptor blocker of third generation with distinct beta-1 with selective and vasodilating properties. A number of experimental and human pharmological studies suggest that the vasodilatation is triggered via increasing vascular NO bioavailabilty which is a consequence of stimulation of NO release and antioxidant properties of this compound. The pharmocological profile is characterised by the significant antihypertensive effect as well as lowering of cardiac pre and after load. Nebivolol is well tolerated and does not appear to significantly influence glucose or plasma lipid metabolism. It is devoid of intrinsic sympathomimetic activity (ISA). This article will review patents, novel composition, pharmacology, haemodynamics, antihypertensive efficiency, metabolic effect and tolerability of nebivolol.
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PMID:Nebivolol: more than a highly selective Beta blocker. 1822 Nov 15

1 In nine hypertensive subjects with angina pectoris, labetalol diminished the incidence of chest pain occurring spontaneously or induced by exercise. 2 Labetalol lowered BP in all subjects. 3 Exercise tolerance at maximum levels was increased by labetalol. 4 Improved cardiac function by labetalol may be related to decreased afterload on the left ventricle, and diminished oxygen utilization by the myocardium.
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PMID:Open evaluation of labetalol in the treatment of angina pectoris occurring in hypertensive patients. 2663 68


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