右美托咪定预处理对大鼠肝脏缺血再灌注后急性肾损伤的影响

吴文峰++++++宁雪++++++尧永华

[摘要] 目的 观察大鼠右美托咪定预处理后对肝脏缺血再灌注后急性肾损伤的的保护作用。 方法 SD雄性大鼠30只，体重220～300 g，随机分为3组：对照组（S组）、肝脏缺血再灌注组（IR组）、右美托咪定组（Dex组）。S组和IR组以1 mL/（kg·h）的速度静滴生理盐水30 min，Dex组给予右美托咪定（6 μg/kg）30 min。间隔2 h后S组仅开腹；IR组和Dex组行肝脏缺血60 min，于再灌注4 h后处死大鼠。测定血清尿素氮（BUN），肌酐（Cr）和肾组织肿瘤坏死因子-α（TNF-α）的浓度，髓过氧化物酶（MPO）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量。取肾组织，光镜下观察病理学改变。 结果 研究中测得IR组血清BUN为（7.58±0.96）mmol/L、Cr为（91.84±10.34）mmol/L，肾组织TNF-α为（238.4±42.7）ng/L、MDA为（3.66±0.95）U/mg prot、SOD为（7.48±1.23）U/mg prot和MPO为（4.73±1.07）U/g。与S组和Dex组比较，IR组血清BUN和Cr的浓度明显升高，差异有统计学意义（P < 0.05），肾组织TNF-α、MDA水平和MPO活性明显升高，差异有统计学意义（P < 0.05），SOD活性明显下降，差异有统计学意义（P < 0.05）。Dex组与S组比较，血清BUN、Cr和肾组织TNF-α、MDA、SOD和MPO活性的差异均无统计学意义（P > 0.05）。Dex组肾组织病理损伤程度与IR组比较明显减轻。 结论 右美托咪定预处理能减轻大鼠肝脏缺血再灌注后的急性肾损伤，其机制可能与抑制炎性因子的分泌，减少氧化应激和中性粒细胞在肾脏的聚集等有关。

[关键词] 右美托咪定；肝脏；预处理；缺血再灌注；肾损伤

[中图分类号] R614 [文献标识码] A [文章编号] 1673-7210（2014）01（c）-0017-03

Effects of Dexmedetomidine preconditioning on acute kidney injury induced by hepatic ischemic-reperfusion

WU Wenfeng NING Xue YAO Yonghua

Department of Anesthesiology， Cancer Hospital of Guangzhou Medical University， Guangdong Province， Guangzhou 510095， China

[Abstract] Objective To investigate the effects of dexmedetomidine preconditioning on acute kidney injury induced by hepatic ischemic-reperfusion. Methods 30 male SD rats weighing 220-300 g were randomly divided into 3 groups（n=10 each）： control group （group S）；ischemic-reperfusion group （group IR） and Dexmedetomidine group （group Dex）. Group S and group IR were injected saline 1mL/（kg·h） for 30 min，Dex group were injectived Dexmedetomidine 6 μg/kg for 30 min. 2 h later， IR group and Dex group animals were administrated hepatic ischemic 60 min. Then， these rats were killed after reperfusion 4 h. The content of serum BUN， Cr and the renal TNF-α， MPO， SOD， MDA were examined. The renal tissue was obtained for microscopic examination. Results In IR group， the concentration of serum BUN and Cr were （7.58±0.96） mmol/L and （91.84±10.34） mmol/L. Renal TNF-α was （238.4±42.7） ng/L， MDA was （3.66±0.95） U/mg prot， SOD was （7.48±1.23） U/mg prot and MPO was （4.73±1.07） U/g. Compared with group S and Dex， the concentration of serum BUN and Cr， renal TNF-α， MDA content and MPO activity significantly increased in IR group， the differences were statistically significant （P < 0.05）. But， renal SOD activity was significantly lower in IR group， the differences were statistically significant （P < 0.05）. Compared with group S， the concentration of serum BUN， Cr， renal TNF-α， MPO content and SOD， MDA activities were no difference in Dex group， the difference was not statistically significant （P > 0.05）. Conclusion Dexmedetomidine preconditioning can reduce acute kidney injury induced by hepatic ischemic-reperfusion through inhibition of TNF-a release and reducing neutrophil infiltration and oxygen radical in renal tissue.endprint