![]() ![]() ![]() ![]() In patients with angina pectoris, plasma concentration measured at 1 hour is linearly related to the oral dose within the range of 50 to 400 mg. Stroke volume, diastolic blood pressure and pulmonary artery end diastolic pressure remained unchanged. In several studies of patients with acute myocardial infarction, intravenous followed by oral administration of metoprolol caused a reduction in heart rate, systolic blood pressure and cardiac output. Proper dosage requires individual titration. Because of variable plasma levels attained with a given dose and lack of a consistent relationship of antihypertensive activity to dose, selection of However, antihypertensive activity does not appear to be related to plasma levels. There is a linear relationship between the log of plasma levels and reduction of exercise heart rate. Equivalent maximal beta-blocking effect is achieved with oral and intravenous doses in the ratio of approximately 2.5:1. When the drug was infused over a 10-minute period, in normal volunteers, maximum beta-blockade was achieved at approximately 20 minutes. After repeated oral dosages of 100 mg twice daily, a significant reduction in exercise systolic blood pressure was evident at 12 hours. For example, a 50% reduction of the maximum effect after single oral doses of 20, 50, and 100 mg occurred at 3.3, 5, and 6.4 hours, respectively, in normal subjects. Significant beta-blocking effect (as measured by reduction of exercise heart rate) occurs within 1 hour after oral administration, and its duration is dose-related. Animal and human experiments indicate that metoprolol slows the sinus rate and decreases AV nodal conduction. Metoprolol has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at doses much greater than required for beta-blockade. (2) In asthmatic patients, metoprolol reduces FEVġ and FVC significantly less than a nonselective beta-blocker, propranolol, at equivalent beta This contrasts with the effect of nonselective (betaĢ) beta-blockers, which completely reverse the vasodilating effects of epinephrine. Myocardial Infarction The precise mechanism of action of metoprolol in patients with suspected or definite myocardial infarction is not known.ġ selectivity is demonstrated by the following: (1) In healthy subjects, metoprolol is unable to reverse the betaĢ-mediated vasodilating effects of epinephrine. However, several possible mechanisms have been proposed: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output (2) a central effect leading to reduced sympathetic outflow to the periphery and (3) suppression of renin activity.Īngina Pectoris By blocking catecholamine-induced increases in heart rate, in velocity and extent of myocardial contraction, and in blood pressure, metoprolol reduces the oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris. Hypertension The mechanism of the antihypertensive effects of beta-blocking agents has not been fully elucidated. This preferential effect is not absolute, however, and at higher plasma concentrations, metoprolol also inhibits betaĢ-adrenoreceptors, chiefly located in the bronchial and vascular musculature.Ĭlinical pharmacology studies have demonstrated the beta-blocking activity of metoprolol, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. ![]() 1-selective (cardioselective) adrenergic receptor blocker. ![]()
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