Dexmedetomidine Attenuates Renal and Myocardial Ischemia/Reperfusion Injury in a Dose-Dependent Manner by Inhibiting Inflammatory Response.

OBJECTIVE

To investigate the effect of dexmedetomidine (DEX) against renal and myocardial ischemia/reperfusion (I/R) injury induced by renal I/R and explore its potential mechanism.

METHODS

Male Wistar rats were randomly allocated to sham, I/R, D1, D2 and D3 group. The sham group received laparotomy without a renal ischemia. I/R injury model was induced by bilateral renal pedicle clamping for 120 min followed by 3 h of reperfusion in I/R, D1, D2 and D3 group. Then D1, D2 and D3 group received DEX of 25 μg/kg, 50 μg/kg and 100 μg/kg by intraperitoneal injection at 30 min from ischemia onset, respectively, and I/R group received normal saline. Renal histopathology, myocardial histopathology and inflammatory cytokines were assessed.

RESULTS

Renal and myocardial tissues were normal in the sham group. Pathological damage showed a trend of I/R>D1>D2>D3 group in renal and myocardial tissue, and the damage was negatively correlated with the dose of DEX. The concentration of creatinine and blood urea nitrogen in serum showed a trend of I/R>D1>D2>D3>sham group. The concentration of tumor necrosis factor α in renal and myocardial tissue showed a trend of I/R>D1>D2>D3>sham group. The concentration of interleukin-10 in renal and myocardial tissue showed a trend of D3>D2>D1>I/R>sham group.

CONCLUSION

DEX could attenuate renal and myocardial I/R injury induced by renal I/R in a dose-dependent manner, at least in part, through its inhibitory effects on inflammatory response.