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

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.