Permissive hypercapnia, instituted via reduction of pressure amplitude on pulmonary tissue protection during high frequency oscillatory ventilation, is not protective in a rat model of acid-induced lung injury.
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Resumo
BACKGROUND
Assuming that HFOV (high frequency oscillatory ventilation) with hypercapnia could be more protective than normocapnia, in a rat model of lung injury, we evaluated the effect of hypercapnic acidosis during HFOV.
METHODS
After inducing lung injury by intratracheal instillation of hydrochloric acid (HCl), we randomly assigned the animals to two groups: in the hypercapnia group (n=9), airway pressure amplitude (Pamp) was titrated to achieve PaCO2 greater than 80 mmHg; in the normocapnia group (n=9), Pamp was titrated to achieve PaCO2 less than 50 mmHg. Hemodynamics, histology, wet-to-dry ratio and inflammatory cytokines were evaluated after all the animals had received HFOV for 5 h.
RESULTS
While the right-lung wet-to-dry ratio in the hypercapnia group was statistically significantly lower than in the normocapnia group (7.70+/-1.31 vs. 8.59+/-0.66, p<0.05), no statistically significant intergroup differences were found for blood pressure, heart rate, alveolar-arterial oxygen gradient, levels of cytokines (TNF-alpha, IL-6 and CINC-1) in bronchoalveolar lavage fluid and serum, and lung histological injury scores.
CONCLUSIONS
Although edema formation was less pronounced in the hypercapnia group, we found no increased numbers of inflammatory cytokines or general histological evidence to suggest that permissive hypercapnia during HFOV was protective.
