The experimental study on infant rabbit lung injury induced by ischemia-reperfusion / 中华胸心血管外科杂志

ABSTRACT

Objective To explore the characteristics of ischemia-reperfusion induced infant lung damage and the potential mechanisms of the injuried.Methods Both infant (15-21 days old) and adult (5-6 months old) rabbits were subjected to either ischemia-reperfusion or sham operation.Ischemia-reperfusion was induced by clamping the right pulmonary hilum for 1 hour and then removal of the clamp for 4 hours under anesthesia.The lung tissue were sampled for histological examination by light and electron microcopies and for biological evaluation of mitochondrial alterations.Production and expression of free radical species-hydroxyl radical (ROS-HR),malondialdehyde (MDA),superoxide dismutase (SOD),glutathione peroxidase (GSH-PX),myeloid differentiation factor-88 (MyD-88),and nuclear factor-κB (NF-κB) in the lung tissue were also examined.In addition,circulating levels of interleukin-β and tumor necrosis factor-α were measured during the ischemia-reperfusion process.Results In comparison to adult lungs,the infant lungs had more increased neutrophil infiltration,edema,swelled alveolar epithelial and endothelial cells,and severer mitochondrial impairment reflected by damage of the inner membrane as well as decrease in the membrane potential after ischemia-reperfusion.The lungs in infant animals subjected to sham operation displayed higher levels of ROS-HR and MDA and lower levels of SOD and GSH-PX than those in adult controls.The lungs in infants with ischemia-reperfusion were found to further produce more ROS-HR,and MDA,and less SOD and GSH-PX than the ischemia-reperfused adult lungs.Moreover,the circulating levels of interleukin-1β and tumor necrosis factor-α were elevated during the period of ischemia-reperfusion,particularly in the infant animals,which appeared to be associated with the expression of MyD-88 and NF-κB in the lungs.Conclusion Lung ischemia-reperfusion causes more severe lung damage in infants than in adults,probably due to combination of low antioxidant capacity and overproduction of ROS in infants.