Intensive care medicine · 2008
Hypercapnic acidosis minimizes endotoxin-induced gut mucosal injury in rabbits.
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Morisaki Hiroshi, Yajima Satoshi, Watanabe Yoko, Suzuki Takeshi, Yamamoto Michiko, Katori Nobuyuki, Hashiguchi Saori, Takeda Junzo
Аннотация
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 F(I)CO(2) 5% under mechanical ventilation to achieve hypercapnia throughout the study periods, whereas the former with F(I)CO(2) 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.
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 F(I)CO(2) 5% under mechanical ventilation to achieve hypercapnia throughout the study periods, whereas the former with F(I)CO(2) 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.