Hypercapnic acidosis attenuates reperfusion injury in isolated and perfused rat lungs*

• DOI: 10.1097/ccm.0b013e318232d776
• Publication Date: 2011-10-04T22:53:33Z
• Authors: Shu-Yu Wu; Chin-Pyng Wu; Bor-Hwang Kang; Min-Hui Li; Shi-Jye Chu; Kun-Lun Huang
• Keywords: Respiratory acidosis

Although ischemia-reperfusion injury is a major determinant of primary graft dysfunction after lung transplantation, an approach to extend preoperative preservation postoperative protection has not yet been defined. The purpose this study was determine the protective effects and signal pathway regulated by hypercapnic acidosis in ischemia-reperfusion-induced injury.Animal study.Animal care facility procedure room medical center.Adult male Sprague-Dawley rats.Lung induced clinically relevant ex vivo animal model. Animals were divided into control group (FICO(2), 5%; n = 6), (ischemia-reperfusion + acidosis) 10%; 6).Ischemia-reperfusion caused significant increases alveolar lavage perfusate tumor necrosis factor-α, inflammatory cell infiltration, tissue malondialdehyde, bronchoalveolar fluid protein concentration lactate dehydrogenase activity, weight gain, infiltration coefficient. Ventilation with 10% CO(2) significantly suppressed response attenuated injury. Our results also showed that inhibited phosphorylation nuclear translocation factor-κB. This associated elevation inhibitor factor-κB-α level reduced IκB kinase-β phosphorylation, suggesting suppression kinase thus IκB-α activation.Hypercapnic may attenuate suppressing activation kinase-nuclear factor-κB pathway.