Ischemic Postconditioning Effects On NF-κB And ICAM-1Expression In Lungs After Cardiopulmonary Bypass In Dogs

Objective: By researching the ischemic postconditioning (IPO)effects on NF-κB andICAM-1expression in dog lungs after cardiopulmonary bypass(CPB), to explore IPOprotective effect on lungs and its action mechanism.Methods: Twelve experimental hybrid dogs were randomly divided into two groups(n=6):left lung ischemia-reperfusion injury of CPB group(group C), ischemic postconditioninggroup (IPO group). Two groups were established left lung ischemia-reperfusion injury ofCPB mode simulating clinical thoracotomy, IPO group was immediately implementischemic postconditioning in the left pulmonary artery open. Samples of lung tissue werecollected at T1(before CPB), T2(open the left pulmonary artery), T3(2h after CPB). Lunginjury was evaluated by the pathological changes and pathological section score at eachtime point. To measure the protein expression changes of the NF-κB and ICAM-1withwestern blot method; and measure the W/D weight ratio of lung tissue; To analyze andcalculate the Respiration index (RI), oxygenation index (OI), dynamic lung compliance(Cd) with the arterial blood samples collected at T1and T3time point.Results:(1) The change of respiratory parameters: Intra-group comparison: After CPB, thePaO2, OI and Cd data of two groups were obviously lower, however, P(A-a)O2and RI dataof two groups were significantly higher(P<0.05); Intergroup comparison: the PaO2, OI andCd of group IPO were obviously higher than group C at T3; while P(A-a)O2and RI showedcontrary trends (P<0.05).(2) Pathology change and the score of lung tissue under optical microscope: After CPB,structural damage of lung tissue was getting worse gradually in two groups. At T1timepoint, the structures of lung tissue were clear for both groups. At T2,the structures of lungtissue were disordered, the alveolar septal were widening, part of the alveolar walls werefractured and damaged, and visible inflammatory cells infiltration appeared. At T3,thestructures of lung tissue were severely disordered, alveolar space collapsed, large sum ofalveolar walls were broken and many inflammatory cells and red blood cells were leakingin Group C; The IPO group also have lung tissue structures’ disorder, alveolar space collapse, inflammatory cells and red blood cells infiltration, but the pathologic damage ofthis group is less than Group C. Pathologic scores: Intra-group comparison: At T2and T3,the two groups pathological score were significantly higher when compared withT1,compared with T2, the score at T3greater than T2(P<0.05); Intergroup comparison: thepathologic scores of IPO group were obviously lower than group C at T3(P<0.05).(3) The W/D weight ratio change of lung tissue: Intra-group comparison: At the time pointof T2and T3,both of the two groups’ W/D ratio were obviously higher than that of T1point,compared with T2, the W/D ratio at T3greater than T2(P<0.05); Intergroup comparison:the W/D in group IPO was significantly lower than group C at T3(P<0.05).(4)The change of expression of NF-κB and ICAM-1in lung tissue: Intra-groupcomparison: At the time point of T2and T3the expression of NF-κB and ICAM-1wassignificantly increased in the two groups compared with T1, compared with T2, theexpression of NF-κB and ICAM-1at T3greater than T2(P<0.05); Intergroup comparison:the expression of NF-κB and ICAM-1in IPO group were significantly lower than groupCat T3(P<0.05).Conclusion:(1) After the CPB in dogs, the expression of NF-κB and ICAM-1in lungtissue were significantly increased, it indicates that NF-κB and ICAM-1could be involvedin the mechanism of CPB induced lung injury;(2)The protective effect of ischemicpostconditioning on lung tissue can inhibit NF-κB activation, decrease the expression ofICAM-1protein, thereby to reduce the dog lung ischemia-reperfusion injury by CPB, andto improve the lung function in dogs, therefore, the IPO has certain protective effect onCPB dog lungs.