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 响简

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220-300g，随机分为3组：对照组（S组）、肝脏缺血再灌注组（IR组）、有美托咪定组（Dex组）。S组和IR组以1mL／（kg·h）的速度静滴生理盐水30min，Dex组给予右美托咪定（6μg／kg）30min。间隔2h后S组仅开腹；IR组和Dex组行肝脏缺血60min，于再灌注4h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／mgprot、SOD为（7．48±1．23）U／mgprot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。

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

Objective To investigate the effects of dexmedetomidine preconditioning on acute kidney injury induced hy 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 Den）. 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 exam- ined. 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/rag 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 concen- tration of serum BUN and Cr, renal TNF-α, MDA content and MPO activity significantly increased in IR group, the dif- ferences 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 ischemie-repeffusion through inhibition of TNF-α release and reducing neutrophil infiltration and oxygen radical in renal tissue.