右美托咪定預處理對大鼠肝臟缺血再灌注后急性腎損傷的影響

吳文峰++++++寧雪++++++堯永華

[摘要] 目的 觀察大鼠右美托咪定預處理后對肝臟缺血再灌注后急性腎損傷的的保護作用。 方法 SD雄性大鼠30只，體重220～300 g，隨機分為3組：對照組（S組）、肝臟缺血再灌注組（IR組）、右美托咪定組（Dex組）。S組和IR組以1 mL/（kg·h）的速度靜滴生理鹽水30 min，Dex組給予右美托咪定（6 μg/kg）30 min。間隔2 h后S組僅開腹；IR組和Dex組行肝臟缺血60 min，于再灌注4 h后處死大鼠。測定血清尿素氮（BUN），肌酐（Cr）和腎組織腫瘤壞死因子-α（TNF-α）的濃度，髓過氧化物酶（MPO）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量。取腎組織，光鏡下觀察病理學改變。 結果 研究中測得IR組血清BUN為（7.58±0.96）mmol/L、Cr為（91.84±10.34）mmol/L，腎組織TNF-α為（238.4±42.7）ng/L、MDA為（3.66±0.95）U/mg prot、SOD為（7.48±1.23）U/mg prot和MPO為（4.73±1.07）U/g。與S組和Dex組比較，IR組血清BUN和Cr的濃度明顯升高，差異有統計學意義（P < 0.05），腎組織TNF-α、MDA水平和MPO活性明顯升高，差異有統計學意義（P < 0.05），SOD活性明顯下降，差異有統計學意義（P < 0.05）。Dex組與S組比較，血清BUN、Cr和腎組織TNF-α、MDA、SOD和MPO活性的差異均無統計學意義（P > 0.05）。Dex組腎組織病理損傷程度與IR組比較明顯減輕。 結論 右美托咪定預處理能減輕大鼠肝臟缺血再灌注后的急性腎損傷，其機制可能與抑制炎性因子的分泌，減少氧化應激和中性粒細胞在腎臟的聚集等有關。

[關鍵詞] 右美托咪定；肝臟；預處理；缺血再灌注；腎損傷

[中圖分類號] R614 [文獻標識碼] A [文章編號] 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