To quantitatively examine and compare the effects of β-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 (Vτ/Tι) were significantly reduced after β-blockade with a concomitant increase in blood PaCO2 (p < 0.01). The timing factor Tι/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 β-blockade. With a stepwise increase in FICO2, the difference in PaCO2 between placebo and bupranolol tended to approach zero, whereas VE and Vτ/Tι remained significantly lower during β-blockade (P < 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 β-blockade and (2) mean inspiratory flow depends also on CO2 elimination characteristics, which are influenced by β-blockade

Keywords:
Control of breathing, β-Adrenergic blockade, Hypercapnia, Breathing pattern, Ventilatory drive
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© 1988 S. Karger AG, Basel
1988
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