Objective
Recent evidence demonstrated that hypercapnic acidosis due to lung protective strategy was not only permissive but also even
therapeutic for injured lung. Since the effects of hypercapnic acidosis on extra-pulmonary organs remain to be clarified,
we tested the hypothesis that hypercapnic acidosis protects gut mucosal barrier function by modulating inflammation in a rabbit
model of endotoxemia.
Design
Prospective randomized animal study.
Setting
University research laboratory.
Subjects
Male New Zealand white rabbits.
Interventions
Thirty-two animals were randomly allocated into two groups: normocapnia (n = 17) and hypercapnia (n = 15). The latter group received FICO2 5% under mechanical ventilation to achieve hypercapnia throughout the study periods, whereas the former with FICO2 0%.
Measurements and results
Arterial blood gas, intramucosal pH (pHi) and portal blood flow were assessed at baseline, 2-h and 4-h infusion of lipopolysaccharide.
At 4 h, ileal myeloperoxidase (MPO) activity and intestinal permeability were measured. The animals in the hypercapnia group
showed apparent hypercapnic acidosis and progressive intramucosal acidosis at 4 h, accompanied by significantly lower intestinal
permeability versus normocapnia group. Ileal MPO activity was comparable between the study groups.
Conclusions
Hypercapnic acidosis attenuates endotoxin-induced gut barrier dysfunction possibly through neutrophil-independent mechanisms.
Keywords Hypercapnia - Bacterial translocation - Intramucosal pH - Myeoloperoxidase