Carbon dioxide--a major determinant of collateral ventilation.

The effects of local or systemic CO2 and changes in pulmonary vascular pressure and flow on the mechanics of collateral ventilation were studied in anesthetized, paralyzed dogs. The resistance to collateral ventilation (Rcoll) decreased by 36.1% when the air being infused into the obstructed segment was replaced with 10% CO2 while the animal was ventilated with air. When the air used to ventilate the animals was replaced with 10% CO2 while air was infused into the segment, Rcoll decreased by 38.6%. When blood flow into the pulmonary artery was stopped (stop flow), pulmonary artery and left atrial pressure decreased. Rcoll increased following stop flow to 125% of control; however, the fall in pulmonary vascular pressures preceded the change in Rcoll. The increase in Rcoll with stop flow was markedly reduced when 10% CO2 was infused into the segment. We conclude that collateral channels respond both to the local infusion of CO2 and to the CO2 concentration in the surrounding lung and/or blood, and that the state of distention of pulmonary vessels surrounding collateral ventilatory channels is not a primary determinant of Rcoll. In addition we conclude that bronchiolar channels rather than interalveolar pores are the pathways for collateral ventilation.