Hypercapnic acidosis attenuates reperfusion injury in isolated and perfused rat lungs.
Crit Care Med
; 40(2): 553-9, 2012 Feb.
Article
em En
| MEDLINE
| ID: mdl-21946657
ABSTRACT
OBJECTIVE:
Although ischemia-reperfusion injury is a major determinant of primary graft dysfunction after lung transplantation, an approach to extend preoperative lung preservation to postoperative protection has not yet been defined. The purpose of this study was to determine the protective effects of and the signal pathway regulated by hypercapnic acidosis in ischemia-reperfusion-induced lung injury.DESIGN:
Animal study.SETTING:
Animal care facility procedure room in a medical center.SUBJECTS:
Adult male Sprague-Dawley rats.INTERVENTIONS:
Lung injury was induced in a clinically relevant ex vivo animal model. Animals were divided into a control group (FICO(2), 5%; n = 6), ischemia-reperfusion group (FICO(2), 5%; n = 6), and hypercapnic acidosis (ischemia-reperfusion + hypercapnic acidosis) group (FICO(2), 10%; n = 6). MEASUREMENTS AND MAINRESULTS:
Ischemia-reperfusion caused significant increases in alveolar lavage and perfusate tumor necrosis factor-α, inflammatory cell infiltration, lung tissue malondialdehyde, bronchoalveolar lavage fluid protein concentration and lactate dehydrogenase activity, lung weight gain, and infiltration coefficient. Ventilation with 10% CO(2) significantly suppressed the inflammatory response and attenuated lung ischemia-reperfusion injury. Our results also showed that hypercapnic acidosis significantly inhibited the ischemia-reperfusion-induced phosphorylation and nuclear translocation of nuclear factor-κB. This was associated with elevation of inhibitor of nuclear factor-κB-α level and reduced IκB kinase-ß phosphorylation, suggesting a suppression of IκB kinase and thus IκB-α activation.CONCLUSIONS:
Hypercapnic acidosis may attenuate lung ischemia-reperfusion injury by suppressing the activation of the IκB kinase-nuclear factor-κB pathway.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Acidose Respiratória
/
Traumatismo por Reperfusão
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Citocinas
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NF-kappa B
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Fator de Necrose Tumoral alfa
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Lesão Pulmonar Aguda
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
/
Risk_factors_studies
Limite:
Animals
Idioma:
En
Revista:
Crit Care Med
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
Taiwan