中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
Chinese Journal of Anesthesiology
2015年
7期
868-871
,共4页
心肺转流术%肺%再灌注损伤%NF-κB%胞间黏附分子1%缺血后处理
心肺轉流術%肺%再灌註損傷%NF-κB%胞間黏附分子1%缺血後處理
심폐전류술%폐%재관주손상%NF-κB%포간점부분자1%결혈후처리
Cardiopulmonary bypass%Lung%Reperfusion injury%NF-kappa B%Intercellular adhesion molecule-1%Ischemic postconditioning
目的 评价缺血后处理对CPB犬肺缺血再灌注损伤时NF-κB及细胞间黏附分子-1(ICAM-1)表达的影响,探讨缺血后处理的肺保护作用及其机制.方法 健康成年杂种犬12只,体重12～15 kg,雌雄不拘,采用随机数字表法分为CPB组和缺血后处理组(IPO组),每组6只.开胸建立CPB,IPO组于开放左肺动脉即刻行缺血后处理(灌注5 min,停灌5 min,重复2次).于CPB前(T1)、开放左肺动脉前(T2)及停机后2h(T3)时取肺组织,光镜下观察病理学结果并行肺损伤评分;采用Western blot法检测左肺组织NF-κB及ICAM-1蛋白表达;并测定左肺湿/干重比(W/D比);于T13时采集股动脉血样行动脉血气分析,计算氧合指数(OI)、呼吸指数(RI)和肺顺应性(Cdyn).结果 与T1时比较,2组T3时OI和Cdyn降低,RI升高,T23时W/D比、肺损伤评分、NF-κB及ICAM-1表达水平升高(P＜0.05);与T2时比较,T3时2组W/D比、肺损伤评分、NF-κB及ICAM-1表达水平升高(P＜0.05).与CPB组比较,IPO组T3时OI和Cdyn升高,RI、W/D比、肺损伤评分、NF-κB及ICAM-1表达水平降低(P＜0.05).结论 缺血后处理通过抑制NF-κB活性,下调ICAM-1表达,减轻CPB犬肺缺血再灌注损伤,改善肺功能.
目的 評價缺血後處理對CPB犬肺缺血再灌註損傷時NF-κB及細胞間黏附分子-1(ICAM-1)錶達的影響,探討缺血後處理的肺保護作用及其機製.方法 健康成年雜種犬12隻,體重12～15 kg,雌雄不拘,採用隨機數字錶法分為CPB組和缺血後處理組(IPO組),每組6隻.開胸建立CPB,IPO組于開放左肺動脈即刻行缺血後處理(灌註5 min,停灌5 min,重複2次).于CPB前(T1)、開放左肺動脈前(T2)及停機後2h(T3)時取肺組織,光鏡下觀察病理學結果併行肺損傷評分;採用Western blot法檢測左肺組織NF-κB及ICAM-1蛋白錶達;併測定左肺濕/榦重比(W/D比);于T13時採集股動脈血樣行動脈血氣分析,計算氧閤指數(OI)、呼吸指數(RI)和肺順應性(Cdyn).結果 與T1時比較,2組T3時OI和Cdyn降低,RI升高,T23時W/D比、肺損傷評分、NF-κB及ICAM-1錶達水平升高(P＜0.05);與T2時比較,T3時2組W/D比、肺損傷評分、NF-κB及ICAM-1錶達水平升高(P＜0.05).與CPB組比較,IPO組T3時OI和Cdyn升高,RI、W/D比、肺損傷評分、NF-κB及ICAM-1錶達水平降低(P＜0.05).結論 缺血後處理通過抑製NF-κB活性,下調ICAM-1錶達,減輕CPB犬肺缺血再灌註損傷,改善肺功能.
목적 평개결혈후처리대CPB견폐결혈재관주손상시NF-κB급세포간점부분자-1(ICAM-1)표체적영향,탐토결혈후처리적폐보호작용급기궤제.방법 건강성년잡충견12지,체중12～15 kg,자웅불구,채용수궤수자표법분위CPB조화결혈후처리조(IPO조),매조6지.개흉건립CPB,IPO조우개방좌폐동맥즉각행결혈후처리(관주5 min,정관5 min,중복2차).우CPB전(T1)、개방좌폐동맥전(T2)급정궤후2h(T3)시취폐조직,광경하관찰병이학결과병행폐손상평분;채용Western blot법검측좌폐조직NF-κB급ICAM-1단백표체;병측정좌폐습/간중비(W/D비);우T13시채집고동맥혈양행동맥혈기분석,계산양합지수(OI)、호흡지수(RI)화폐순응성(Cdyn).결과 여T1시비교,2조T3시OI화Cdyn강저,RI승고,T23시W/D비、폐손상평분、NF-κB급ICAM-1표체수평승고(P＜0.05);여T2시비교,T3시2조W/D비、폐손상평분、NF-κB급ICAM-1표체수평승고(P＜0.05).여CPB조비교,IPO조T3시OI화Cdyn승고,RI、W/D비、폐손상평분、NF-κB급ICAM-1표체수평강저(P＜0.05).결론 결혈후처리통과억제NF-κB활성,하조ICAM-1표체,감경CPB견폐결혈재관주손상,개선폐공능.
Objective To evaluate the effects of ischemic postconditioning on nuclear factor kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) expression during lung ischemia-reperfusion (I/R) injury in a dog model of cardiopulmonary bypass (CPB), and further investigate the pulmonary protection induced by ischemic postconditioning and the underlying mechanism.Methods Twelve adult mongrel dogs of both sexes, weighing 12-15 kg, were randomly divided into either CPB group or ischemic postconditioning group (IPO group) using a random number table, with 6 dogs in each group.CPB was established after the chest was opened in dogs anesthetized with pentobarbital sodium.Ischemic postconditioning was induced by 2 cycles of 5 min reperfusion followed by 5 min ischemia immediately after occlusion of the left pulmonary artery was released in group IPO.Before CPB (T1), before occlusion of the artery was released (T2) , and at 2 h after termination of CPB, lung specimens were obtained for examination of pathological changes which were scored (with light microscope) and for determination of the expression of NFκB and ICAM-1 (using Western blot) and wet/dry lung weight ratio (W/D ratio) in left lung tissues.Blood samples were collected from femoral arteries at T1 and T3 for blood gas analysis, and oxygenation index (OI), respiration index (RI) and dynamic lung compliance (Cdyn) were calculated.Results OI and Cdyn were significantly decreased, and RI was increased at T3 , and W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were increased at T2,3 than at T1 in the two groups.W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were significantly higher at T3 than at T2 in the two groups.Compared with group CPB, OI and Cdyn were significantly increased, and R1, W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were decreased at T3 in group IPO.Conclusion Ischemic postconditioning up-regulates the expression of ICAM-1 through inhibiting NF-κB activity, thus reducing lung I/R injury induced by CPB and improving the lung function in dogs.
