摘要
目的探讨缺血后处理对大鼠在体肺缺血-再灌注损伤中炎症反应的影响。方法将40只SD大鼠随机分成假手术组(S组)、缺血-再灌注30 min组(I/R-30组)、缺血-再灌注120 min组(I/R-120组)、缺血后处理30 min组(IPO-30)和缺血后处理120 min组(IPO-120),每组8只。S组完成左侧开胸手术操作,肺门过阻断带,但肺门未阻断;I/R组拉紧肺门阻断带阻断左肺门,造成左肺缺血1 h,然后松开阻断带再灌注30 min和120 min(即I/R-30组和I/R-120组);IPO组在1 h的缺血之后再灌注开始前先进行10 s的缺血及10 s的再灌注(共3个循环,持续1 min),然后是与I/R组同样的30 min和120 min的长时间持续灌注(即IPO-30组和IPO-120组)。测定各组肺组织中白细胞介素10(IL-10)及血浆可溶性细胞间粘附分子1(sICAM-1)的水平。观察肺组织的病理形态变化并进行弥漫性肺泡损伤(DAD)评分。结果 I/R-30组和I/R-120组血浆中sICAM-1水平比S组显著升高[(2.140±0.250)μg/L vs(.0.944±0.188)μg/L,P=0.003;(2.191±0.230)μg/L vs(.0.944±0.188)μg/L,P=0.003],肺组织中IL-10水平亦明显高于S组[(15.922±0.606)pg/mg pro vs.(7.261±0.877)pg/mg pro,P=0.037;(17.421±1.232)pg/mg pro vs.(7.261±0.877)pg/mg pro,P=0.042],组织损伤明显。缺血后处理干预后,IPO-30组和IPO-120组血浆sICAM-1水平与相应I/R组各时间点相比显著降低[(1.501±0.188)μg/L vs(.2.140±0.250)μg/L,P=0.038;(1.350±0.295)μg/L vs(.2.191±0.230)μg/L,P=0.005],而IL-10水平显著升高[(20.950±1.673)pg/mg pro vs.(15.922±0.606)pg/mg pro,P=0.008;(25.334±1.173)pg/mg pro vs.(17.421±1.232)pg/mg pro,P=0.006],DAD评分显著降低[6.8±1.4 vs.11.5±1.9,P=0.007;7.5±1.6 vs.13.2±1.7,P=0.005],肺组织损伤较I/R组显著减轻。结论缺血后处理可能通过抑制炎症反应从而减轻肺缺血-再灌注损伤。
Objective To investigate the effects of ischemic postconditioning （IPO） on inflammatory response inischemia-reperfusion （IR） injury of rat lungs in vivo. Methods Forty SD rats were randomly divided into 5 groups inclu-ding a sham surgery group （S group），a 30-minute IR group （I/R-30 group），a 120-minute IR group（IR-120 group），a 30-minute IPO group （IPO-30 group），and a 120-minute IPO group （IPO-120 group）. There were 8 rats in each group. All therats received left thoracotomy after anesthesia. In the sham surgery group，a line was only placed around the left hilum butnot fastened. In the I/R-30 group and I/R-120 group，a line was fastened to block the blood flow of the left lung for 1 hour，then loosened for reperfusion for 30 minutes and 120 minutes respectively. In the IPO-30 group and IPO-120 group，afterblocking the blood flow of the left lung for 1 hour，the left hilum was fastened for 10 seconds and loosened for 10 seconds（repeating 3 times for 1 minute），then the line was loosened for 30 minutes and 120 minutes respectively. The levels of interleukin-10 （IL-10） in lung tissues and soluble intercellular adhesion molecule-1 （sICAM-1） in plasma were measured. Histopathological changes of lung tissues were observed and diffuse alveolar damage （DAD） scores was calculated.Results The levels of plasma sICAM-1 in the I/R-30 group and I/R-120 group were significantly higher than that of S group ［（2.140±0.250）μg/L vs. （0.944±0.188）μg/L，P=0.003；（2.191±0.230）μg/L vs. （0.944±0.188）μg/L，P=0.003］. IL-10levels in lung tissues in the I/R-30group and I/R-120 group were also significantly higher than that of S group［（15.922±0.606）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.037；（17.421±1.232）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.042］. Pathologic lesions of lung tissues in the I/R-30 group and I/R-120 group were more severe than that of S group. After IPO, plasma sICAM-1 levels in the IPO-30 group and IPO-120 group were significantly lower than those in the I/R-30group and I/R-120 group respectively ［（1.501±0.188）μg/L vs.（2.140±0.250）μg/L，P=0.038；（1.350±0.295）μg/L vs.（2.191±0.230）μg/L，P=0.005］. IL-10 levels in lung tissues in the IPO-30 group and IPO-120 group were significantly higherthan those in the I/R-30 group and I/R-120 group respectively ［（20.950±1.673）pg/mg pro vs.（15.922±0.606）pg/mgpro，P=0.008；（25.334±1.173）pg/mg pro vs.（17.421±1.232）pg/mg pro，P=0.006］. DAD scores in the IPO-30 group andIPO-120 group were significantly lower than those in the I/R-30 group and I/R-120 group respectively ［6.8±1.4 vs. 11.5±1.9，P=0.007；7.5±1.6 vs. 13.2±1.7，P=0.005］. Pathological lesions of the lung tissues of IPO groups were less severe than those of I/R groups. Conclusion IPO can attenuate IR injury by inhibiting inflammatory response in rat lungs.
出处
《中国胸心血管外科临床杂志》
CAS
2013年第6期705-709,共5页
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery
基金
福建省医学创新课题(2009-CXB-62)
汕头市重点科技计划项目(汕府科[2010]63号)~~
