Differential effects of beta-adrenergic blockade on P0.1 and mean inspiratory flow

To quantitatively examine and compare the effects of beta-adrenergic blockade on ventilation, we studied 20 healthy volunteers during inhalation of room air and at steady state CO2 (2.0, 4.4, 6.0%) following a single oral dose of bupranolol (vs. placebo). During room air breathing, minute ventilation (VE) and mean inspiratory flow (VT/TI) were significantly reduced after beta-blockade with a concomitant increase in blood PaCO2 (p less than 0.01). The timing factor TI/Ttot and mouth occlusion pressure P0.1 remained unchanged. These differences were, as shown from calculated effective alveolar ventilation, mainly attributed to a decrease in physiological dead space ventilation following beta-blockade. With a stepwise increase in FICO2, the difference in PaCO2 between placebo and bupranolol tended to approach zero, whereas VE and VT/TI remained significantly lower during beta-blockade (P less than 0.05). In contrast, no difference existed in P0.1 between bupranolol and placebo. We suggest that (1) respiratory drive assessed by P0.1 is unaffected by beta-blockade and (2) mean inspiratory flow depends also on CO2 elimination characteristics, which are influenced by beta-blockade.