Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury

- Therapeutic hypercapnia with and without acidosis reduced diffuse alveolar damage.
- Hypercapnia decreased interleukin-6 and interleukin-1β expressions.
- Hypercapnia reduced fibrogenesis.
- Hypercapnia, regardless of acidosis, decreased lung and kidney cell apoptosis.

We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n = 7/group): (1) normocapnia (NC, PaCO2 = 35-45 mmHg), ventilated with 0.03%CO2 + 21%O2 + balanced N2; (2) hypercapnic acidosis (HC, PaCO2 = 60-70 mmHg), ventilated with 5%CO2 + 21%O2 + balanced N2; and (3) buffered hypercapnic acidosis (BHC), ventilated with 5%CO2 + 21%O2 + balanced N2 and treated with sodium bicarbonate (8.4%). The remaining seven animals were not mechanically ventilated (NV). The mRNA expression of interleukin (IL)-6 (p = 0.003), IL-1β (p < 0.001), and type III procollagen (PCIII) (p = 0.001) in lung tissue was more reduced in the HC group in comparison with NC, with no significant differences between HC and BHC. Lung and kidney cell apoptosis was reduced in HC and BHC in comparison with NC and NV. In conclusion, in this experimental ALI model, hypercapnia, regardless of acidosis, reduced lung inflammation and lung and kidney cell apoptosis.