Propranolol does not affect the oxidative burst of rat neutrophils or complement serum opsonizing capacity in in vivo and in vitro experiments

Abstract

Propranolol is a ß-adrenergic antagonist used for the treatment of a variety of cardiac conditions and has a palliative value when used in situations in which adrenergic signals and symptoms are involved. It is used as a co-adjuvant in hyperthyroidism to decrease heart rate and output, as well as the tremor. The aim of this work was to study the effect of propranolol treatment on the oxidative burst of rat peripheral blood neutrophils and on the complement system.

In the in vivo study, Wistar male rats were treated with propranolol by gavage for 16 days with 220 or 440 μg/animal/day. These doses are equivalent to 80 or 160 mg/adult human (~70 day/kg), respectively. Neutrophils were obtained and stimulated with opsonized immune complexes (opIC). The oxidative burst of control (from water treated rats) or propranolol-treated rat cells was measured by luminol- and lucigenin-dependent chemiluminescence (CL). The CL of treated rat neutrophils was not affected by any of the propranolol doses studied when compared to the control responses.

In the in vitro study whole blood and serum from Wistar male rats were incubated for 1 h at 37C° with propranolol at three different concentrations (17.5, 35 and 70 μg/mL). After incubation, neutrophils were isolated from whole blood and stimulated with opIC while treated sera were used to opsonize IC. IC opsonized with treated sera were used to stimulate neutrophils from normal rats. In both cases oxidative burst was measured by luminol- and lucigenin-dependent CL. No differences in responses or activities were detected between in vitro treated neutrophils or sera and their respective controls.

These results suggest that this drug, at the concentrations studied and with the experimental approach used, had no effect on the oxidative burst during phagocytosis of opIC or on the complement opsonization capacity of the sera.