Effect of exogenous hypercapnia on lung's pro‐ and anti‐inflammatory cytokines during development of pulmonary oxygen toxicity in neonatal rats

Exogenous Hypercapnia, the intentional addition of CO2 to the ambient gas, is being explored as a possible means of protecting the lung from ongoing damage due to hyperoxia or ventilator‐induced lung injury. We studied the effect of hypercapnia on lung's inflammatory cytokines during the development of pulmonary oxygen toxicity in one‐day old rats exposed to air (normoxia; 21% O2), Hyperoxia (>98% O2), or Hyperoxia/Hypercarbia (HHC; 95% O2 + 5%CO2), for 96 hours (n=15/group). After euthanasia, the lungs were homogenized for determination of IL‐1 beta, IL‐6, TNF‐alpha, and IL‐10 content by ELISA procedures. Production of IL‐1‐beta and TNF‐alpha were significantly reduced during hyperoxia and HHC, as compared to normoxia (P<0.001; ANOVA followed by Tukey‐Kramer). These decreases were more severe in the HHC rats as compared to hyperoxia‐treated rats (p<0.05). IL‐10 production was significantly increased only in hyperoxic rats, as compared to normoxia. No significant changes occurred in IL‐6 production in all groups, compared to each other. These data suggest that exogenous hypercapnia may modulate the onset of pulmonary oxygen toxicity in neonatal rats by modifying inflammatory response to hyperoxia.