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目的:探讨依达拉奉对犬自体肾移植缺血再灌注损伤的影响及机制。方法:将18只体重匹配的健康杂种犬随机分为假手术组(S组)、依达拉奉组(ED组)、生理盐水组(PS组),每组各6只。S组仅进行肾手术切除;ED组在阻断前在供体静脉内注入依达拉奉10 mg/kg,然后使用200 mL加入依达拉奉10 mg/kg的UW液灌洗供体肾并在同样的保存液中保存供体肾8小时,且再灌注开始时立即在受体静脉内给予依达拉奉10 mg/kg;PS组同法使用相同体积的生理盐水。再灌注4 h后检测MDA、MPO、SOD、iNOS、eNOS等活性;术后24 h检测血清肌酐(Cr)、尿素氮(BUN)浓度;光镜下观察肾组织病理学改变。结果:PS组MDA显著高于S组及ED组(P<0.05),PS组MPO含量亦低于S组及ED组(P<0.05)。PS组SOD、eNOS含量显著低于于S组及ED组(P<0.05),PS组iNOS含量高于S组及ED组(P<0.05),ED组的肾损伤明显减轻。结论:依达拉奉能减轻肾移植缺血再灌注损伤,其机制可能与减轻肾脂质过氧化反应有关。
Objective: To investigate the effect and mechanism of edaravone on ischemia-reperfusion injury of autologous renal transplantation in dogs. Methods: Eighteen body weight-matched healthy mongrel dogs were randomly divided into sham-operation group (S group), edaravone group (ED group) and saline group (PS group) In group S, only renal resection was performed. In ED group, edaravone 10 mg / kg was injected into donor vein immediately before blockade, and then donor kidney was irrigated with 200 mL UW solution with edaravone 10 mg / kg Donor kidneys were preserved for 8 hours in the same preservation solution and edaravone 10 mg / kg was intravenously administered to recipients immediately after reperfusion; the same volume of saline was used in the same manner as in PS group. The activities of MDA, MPO, SOD, iNOS and eNOS were detected 4 h after reperfusion. Serum creatinine (Cr) and urea nitrogen (BUN) concentrations were measured at 24 h after operation. Pathological changes of renal tissue were observed under light microscope. Results: The MDA level in PS group was significantly higher than that in S group and ED group (P <0.05). The MPO level in PS group was also lower than that in S group and ED group (P <0.05). The levels of SOD and eNOS in PS group were significantly lower than those in S group and ED group (P <0.05). The content of iNOS in PS group was higher than that in S group and ED group (P <0.05). Conclusion: Edaravone can reduce ischemia-reperfusion injury after renal transplantation, the mechanism may be related to the reduction of renal lipid peroxidation.