CAJ | 학술논문

目的探讨远程缺血预处理(RIPC)对肝缺血再灌注损伤(HIRI)的影响及其机制.方法将36只雄性SD大鼠随机分为3组:假手术组(Sham组)仅行开腹及肝门分离;缺血再灌注模型组(IR组)采用Pringle's法阻断肝门15 min,再灌注2h;缺血预处理组(RIPC组)首先阻断脾动脉15 min,放开15 min,后其操作同IR组.各组大鼠在再灌注2h后分别取门静脉血清测谷丙转氨酶(ALT)、谷草转氨酶(AST);取肝组织作病理学检查、免疫组织化学法肿瘤坏死因子-α(TNF-α)和P-选择素测定.结果与Sham组比较,血清ALT、AST水平在IR组[(466.75±89.45)、(782.25±87.71) U/L)]和RIPC组[(231.87 ±50.80)、(326.75 ±19.12) U/L]明显升高(P＜0.05);肝组织病理损伤评分升高(P＜0.05);肝组织内TNF-α和P-选择素表达升高(p＜0.05).其中上述指标在RIPC组中水平较IR组均明显降低(P＜0.05).结论脾脏缺血预处理可减轻HIRI,分析其原因可能是通过减少黏附因子的表达,减轻中性粒细胞的聚集,从而减少炎性损伤而发挥作用.
목적 탐토원정결혈예처리(RIPC)대간결혈재관주손상(HIRI)적영향급기궤제.방법 장36지웅성SD대서수궤분위3조:가수술조(Sham조)부행개복급간문분리;결혈재관주모형조(IR조)채용Pringle's법조단간문15 min,재관주2h;결혈예처리조(RIPC조)수선조단비동맥15 min,방개15 min,후기조작동IR조.각조대서재재관주2h후분별취문정맥혈청측곡병전안매(ALT)、곡초전안매(AST);취간조직작병이학검사、면역조직화학법종류배사인자-α(TNF-α)화P-선택소측정.결과 여Sham조비교,혈청ALT、AST수평재IR조[(466.75±89.45)、(782.25±87.71) U/L)]화RIPC조[(231.87 ±50.80)、(326.75 ±19.12) U/L]명현승고(P＜0.05);간조직병리손상평분승고(P＜0.05);간조직내TNF-α화P-선택소표체승고(p＜0.05).기중상술지표재RIPC조중수평교IR조균명현강저(P＜0.05).결론 비장결혈예처리가감경HIRI,분석기원인가능시통과감소점부인자적표체,감경중성립세포적취집,종이감소염성손상이발휘작용.
Objective To investigate the effect and mechanism of remote ischemic preconditioning on hepatic ischemia-reperfusion injury.Methods Thirty six SD rats were divided into three group randomly:Sham-operated group (Sham group),ischemia-reperfusion group (IR group:produced by total inflow occlusion for 15 min),and remote ischemic preconditioning group [remote ischemic preconditioning (RIPC) group:induced with 15 min ischemia of spleen before hepatic ischemia].Serum aminotransferases [alanine aminotransferase (ALT),aspartate aminotransferase (AST)] and tumor necrosis factor (TNF)-α,P-selectin in liver were measured after reperfusion for 2 h.Results Compared with the Sham group,the level of ALT,AST and the pathological injury scores were significantly increased in the IR [(466.75 ± 89.45),(782.25 ±87.71) U/L and RIPC (231.87 ±50.80),(326.75 ± 19.12) U/L] groups.TNF-α and p-selectin expression were high when IR only as well.These variables were significant decreased in RIPC group.Conclusion Remote ischemic preconditioning of spleen decreases the reperfusion injury during hepatic ischemia which may be caused by the decrease of pro-inflammatory and activity of neutophils.