Effect of dexmedetomidine on kidney injury induced by liver ischemia-reperfusion in rats

Objective To evaluate the effect of dexmedetomidine on kidney injury induced by liver ischemia-reperfusion (I/R) in rats. Methods Twenty-four healthy male Sprague-Dawley rats, weighing 220-250 g, aged 8-10 weeks, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S); liver I/R group (group I/R); dexmedetomidine group (group D). In group I/R, liver I/R model was established by clamping the portal vein, hepatic artery, supra- and infra-hepatic vena cava for 40 min, followed by 6 h of reperfusion in anesthetized rats.In group D, dexmedetomidine 100 μg/kg was injected intraperitoneally at 30 min before skin incision.The equal volume of normal saline was given instead of dexmedetomidine in S and I/R groups.At 6 h of reperfusion, blood samples were collected from the infra-hepatic vena cava for determination of blood urea nitrogen (BUN) and creatinine (Cr) concentrations (by automatic biochemical analyzer) and tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) concentrations in serum (by enzyme-linked immunosorbent assay). After blood sampling, the rats were sacrificed, and kidneys were harvested for examination of histopathological changes (with light microscope) and for determination of malondialdehyde (MDA) content (using thiobarbituric acid method) and superoxide dismutase (SOD) activity (by xanthine oxidase method), expression of activated caspase-3 (by immuno-histochemistry), and apoptotic cells (using TUNEL). Apoptotic rate was calculated. Results Compared with group S, the serum BUN, Cr and TNF-α concentrations were significantly increased, the concentration of serum IL-10 was decreased, the MDA content and apoptotic rate were increased, the SOD activity was decreased, and the expression of activated caspase-3 was up-regulated in I/R and D groups (P<0.05). Compared with group I/R, the serum BUN, Cr and TNF-α concentrations were significantly decreased, the concentration of serum IL-10 was increased, MDA content and apoptotic rate were increased, the SOD activity was decreased, the expression of activated caspase-3 was down-regulated (P<0.05), and the histopathological changes of renal tissues were attenuated in group D. Conclusion Dexmedetomidine can reduce kidney injury induced by liver I/R in rats, and the mechanism is probably related to inhibition of inflammatory responses, lipid peroxidation and cell apoptosis. Key words: Dexmedetomidine; Reperfusion injury; Liver; Kidney