[Effect of bupranolol on hypoxic respiratory stimulation in healthy probands].

To determine whether hypoxic ventilatory response results, in part, from concomitant systemic sympathoadrenal stimulation, we studied ventilation in 20 healthy subjects before and after administration of a beta-blocking agent. A single oral dose of 100 mg bupranolol (vs placebo) significantly lowered minute ventilation from 9.4 +/- 0.7 to 8.3 +/- 0.2 l/min (mean +/- SEM) during normoxia, and from 10.8 +/- 0.8 to 8.9 +/- 0.2 l/min, when 11% O2 was inhaled. In our study, there were marked oscillations of ventilation on changing from room air to hypoxic breathing and back. They were ascribed to the preceding sampling of specimens for blood gas analysis. However, bupranolol had no influence on these transients. Bupranolol also had only slight cardiocirculatory effects during normoxia and did not prevent significant T-wave flattening, increase in heart rate, and fall in diastolic blood pressure during hypoxia. However, it did block the hypoxic increase in systolic blood pressure. From our results we suggest that (1) in spontaneously breathing conscious subjects, hypoxia-induced hyperventilation is also due to hypoxic sympathoadrenal activity and individual mental state, and (2) these influences do not affect all aspects of the cardiocirculatory response.