Propranolol-vagal-alveolar CO2 interactions on collateral gas flow in dog lungs

Abstract

The mechanical properties of a collaterally ventilating lung segment were studied in 18 anesthetized paralyzed mongrel dogs artificially ventilated with room air end-tidal CO2 fraction = 5%. Nine dogs were pretreated with propranolol, and nine dogs were not. With 0, 5, or 12% CO2 in O2 flowing into the segment, steady-state resistance of segmental airways (Rss) and time for 90% pressure equilibration (T90) between the segment and airway opening after flow was discontinued were determined at functional residual capacity with the vagus nerve ipsilateral to the segment intact, sectioned, or electrically stimulated. Vagal stimulation increased Rss and T90 at all CO2 levels, whereas unilateral vagotomy had no effect. Propranolol treatment enhanced the increase in Rss caused by vagal stimulation at low but not at high CO2 levels, suggesting that high CO2 mimics the effect of propranolol on Rss. High levels of CO2 did not have the same effect as propranolol on T90, propranolol treatment reducing the increase in T90 caused by vagal stimulation at high but not at low CO2 levels. These results demonstrate that local changes in alveolar CO2 tensions modify but do not abolish the effect of vagal stimulation on collateral ventilation.