Lung inflation with carbon monoxide during the cold ischemia phase ameliorates lung ischemia-reperfusion injury / 中华器官移植杂志

ABSTRACT

Objective To observe the effects and mechanism of lung inflation with carbon monoxide (CO) during the cold ischemia phase on lung ischemia-reperfusion injury (IRI) after rat lung transplantation.Method Twenty-four pairs of SD rats were selected to establish the model of lung transplantation,and random number method was used to divide 24 donors into 3 groups with 8 rats in each group.(1) CO inflation group (CO group):During the cold ischemia phase,500 ppm CO +volume fraction 40％ O2 + N2 was used for lung inflation,and the volume was 5 mL/kg;(2) O2 inflation group (O2 group):During the cold ischemia phase,volume fraction 40％ O2 + volume fraction 60％ N2 was used for lung inflation;(3) Control group:The lung was deflated during the cold ischemia phase.The gas was replaced every 30 min in the CO and O2 groups,and the lung transplantations were performed after 180 min of cold ischemia.The arterial blood gas analysis was performed at baseline,3 min after reperfusion,and 60,120,and 180 min after reperfusion.The recipient serum levels of relative inflammatory factors,lung tissue cell apoptosis and nuclear factor kappa B (NF-κB) protein expression were detected after 180 min of reperfusion.Result As compared with the control group (238 ± 61 mm Hg),the oxygenation index in the O2 group (293 ± 78 mm Hg) and CO group (361 ± 48 mm Hg) was increased (P＜0.05),and as compared with the O2 group,that in the CO group was increased (P＜0.05).Furthermore,as compared with the control group,the interleukin (IL)-8,tumor necrosis factor (TNF)-α,and cell apoptosis in the O2 group and CO group were decreased significantly,and as compared with the O2 group,those in the CO group and NF-κB protein expression were significantly decreased (P＜0.05).Conclusion Lung inflation with CO during the cold ischemia phase ameliorated the rat lung IRI via reducing the inflammatory response and cell apoptosis mediated by the NF-κB pathway.