Effects of intravenous propranolol and metoprolol and their interaction with isoprenaline on pulmonary function, heart rate and blood pressure in asthmatics

Abstract

The effects of propranolol (0.06 mg/kg i.v.), the selective beta1-receptor antagonist metoprolol (0.12 mg/kg i.v.) and a placebo on pulmonary function, heart rate and blood pressure have been compared in asthmatics. The interaction of these drugs with increasing doses of isoprenaline on the same variables was also studied. The two beta-blockers reduced resting heart rate to the same extent, indicating the same degree of blockade of cardiac beta-receptors. Both beta-blockers reduced the basal forced expiratory volume in one second (FEV1), and the effect tended to be more pronounced after propranolol. Isoprenaline caused a dose-dependent increase in FEV1 and vital capacity (VC). These effects were almost completely blocked by propranolol, whereas after metoprolol the changes approached that of the placebo. The isoprenaline-induced increase in heart rate and fall in diastolic blood pressure was also inhibited to a considerably greater extent by propranolol than by metoprolol. The results show a selectivity of metoprolol for so-called beta1-receptors and indicate that metoprolol may be used in asthmatics provided that it is combined with beta2-receptor-stimulating drugs.

Bronchial and cardiac beta‐adrenoceptor blockade‐a comparison of atenolol, acebutolol and labetalol.

“…This approach has been used in man to assess cardiac 0-adrenoceptor blockade by measuring the heart rate response to increasing doses of intravenous isoprenaline (Paterson etal, 1970;Cleaveland, Rango & Shand, 1972). A similar approach to the assessment of bronchial ,B-adrenoceptor blockade has been attempted in patients with asthma by measuring the FEV1 response to increasing intravenous doses of isoprenaline before and after P-adrenoceptor antagonists (Johnsson, Svedmyr & Thiringer, 1975;Thiringer & Svedmyr, 1976 with initial airway diameter (Benson, 1975).…”

Comparison of atenolol and oxprenolol in patients with angina or hypertension and co‐existent chronic airways obstruction.

“…(Bernecker & Roetscher, 1970;Waal-Manning & Simpson, 1971;Formgren, 1972), acebutolol (Skinner & Palmer, 1974) and metoprolol (Johnsson, Svedmyr & Thiringer, 1975)], atenolol does pose a potential hazard to asthmatics. Skinner & Palmer (1974) conclude that any ,-adrenoceptor blocking drug must be used with extreme caution in asthmatics, and Johnsson et al (1975) combined with afl2-receptor-stimulating drug.…”

“…Kumana, Kaye, Leighton, Turner & Hamer (1975) used vigorous exercise to achieve this, and under these conditions showed no difference between propranolol and acebutolol. Johnsson et al (1975) used isoprenaline infusion and demonstrated that metoprolol permitted an excellent bronchodilator response in contrast to propranolol which almost completely blocked this effect. Similarly Skinner & Palmer (1974), using isoprenaline aerosol, demonstrated that practolol was cardioselective and acebutolol relatively less selective.…”

The assessment of beta‐adrenoceptor blocking drugs in man.

“…They Isoprenaline testing has recently been extended to include measurement of respiratory function for the assessment of cardioselectivity. Graded doses of isoprenaline by continuous intravenous infusion have been employed in asthmatic patients in whom FEV1, heart rate and blood pressure by sphygmomanometry have been recorded (Johnsson, Svedmyr & Thiringer, 1975;Thiringer & Svedmyr, 1976). In both studies metoprolol and propranolol were compared; in one of them, practolol was also included.…”