Evidence for a Dilator Action of Carbon Dioxide on the Pulmonary Vessels of the Cat
Isolated cat lungs perfused at constant flow (75 ml/min per kg total body weight) were ventilated with gases of varying CO2 content (0 to 10%), 20% O2, and the balance N2. Tidal volume was constant, and airway pressure did not change. Left atrial pressure was held constant, and changes in pulmonary artery pressure (PPA) were taken to reflect changes in pulmonary vascular resistance. Progressive hypercapnia (Pco2 = 0 to 60 mm Hg) resulted in an increase in PPA as pH decreased. Equivalent degrees of acidosis, produced by the infusion of 0.3 N lactic acid, resulted in a higher PPA. Changes in PPA produced by lactic acid were reversible with 0.89 M sodium bicarbonate. With Pco2 constant, and pH changed by lactic acid or sodium bicarbonate infusion, PPA was higher in lungs ventilated with room air (Pco2 = 0) than in those ventilated with 5 or 10% CO2 (Pco2 = 30 or 60 mm Hg) at the same hydrogen ion concentration of the perfusate. These findings can be explained by two opposing actions of CO2 on pulmonary vessels: a dilator action due to the direct effect of CO2 and a constrictor action caused by the increase in hydrogen ion concentration.
- isolated perfused lungs
- respiratory acidosis
- metabolic acidosis
- pulmonary vasomotor activity
- pulmonary vascular resistance
- Accepted January 10, 1968.
- © 1968 American Heart Association, Inc.