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. It is concluded 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, it is concluded that bronchiolar channels rather than interalveolar pores are the pathways for collateral ventilation.