Alveolar epithelium is exposed to high CO2 tensions (hypercapnia) in patients with COPD and during permissive hypercapnia in mechanically ventilated subjects. Recently, some reports propose that hypercapnia could be beneficial in the treatment of ALI/ARDS. However, more recently new data has been presented suggesting that hypercapnia may have deleterious effects on the pulmonary epithelium. The objective of our investigation was to determine the effects of hypercapnia on alveolar epithelial function.
Alveolar fluid reabsorption (AFR) was assessed during hypercapnia with normal and acid pH as compared to metabolic acidosis in the isolated rat lung model. In parallel, Na,K-ATPase activity and protein abundance in alveolar type II cell cultures was evaluated.
Hypercapnia decreased AFR by ∼ 60% (pCO2 ∼ 80 mmHg, pH = 7.15). With high pCO2 even at normal pH (7.40) alveolar fluid reabsorption was decreased but not during metabolic acidosis (pH 7.2 and normal PCO2). The deleterious effect of hypercapnia on AFR was not associated with changes of intracellular pH and reversed when pCO2 was normalized. The Na,K-ATPase activity and protein abundance was decreased in alveolar epithelial cells exposed to hypercapnia but not metabolic acidosis.
Our data suggest that hypercapnia but not metabolic acidosis impairs alveolar fluid reabsorption via an endocytosis-mediated process of the Na,K-ATPase in alveolar epithelial cells leading to decreased Na,K-ATPase activity.
We reason that permissive hypercapnia may have deleterious effects on alveolar epithelial function and the ability of the lungs to clear edema in mechanically ventilated patients.
Arturo Briva, None.