Hypercapnic acidosis minimizes endotoxin-induced gut mucosal injury in rabbits View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-01

AUTHORS

Hiroshi Morisaki, Satoshi Yajima, Yoko Watanabe, Takeshi Suzuki, Michiko Yamamoto, Nobuyuki Katori, Saori Hashiguchi, Junzo Takeda

ABSTRACT

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. More... »

PAGES

129-135

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00134-008-1212-7

DOI

http://dx.doi.org/10.1007/s00134-008-1212-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1014863945

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18626629


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43 schema:description 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.
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