The Protective Mechanism of Dexmedetomidine on Renal in Hemorrhagic Shock

Abstract

Objective. To explore the protective effect of dexmedetomidine on renal function in patients with hemorrhagic shock and its possible mechanism. Methods. Seventy patients with traumatic hemorrhagic shock requiring surgical treatment were randomly divided into the control group (group C) and the dexmedetomidine group (group D), with 35 patients in each group. Patients in both groups were actively treated with volumetric resuscitation while surgical hemostasis. Group D was given dexmedetomidine 0.5 μg/kg before skin incision after anesthesia induction, for 10 min, followed by intravenous infusion at a rate of 0.4 μg·kg-1·h-1 until 30 min before surgery, and group C was given equal volume of normal saline before skin resection (H1). Venous blood was collected 2 h (H2) and 4 h (H4) after skin resection, and plasma levels of BUN, creatinine (SCr), lipid peroxides (MDA), and inflammatory mediators IL-6 and IL-8 were measured on the 1st and 2nd day after surgery. Results. Compared with H1, BUN and SCr levels had no significant difference at 2 h and 4 h after skin resection but significantly decreased at 1 and 2 postoperative days (D1) ( $P<0.05$ ). There were significant differences in MDA, IL-6, and IL-8 at 2 and 4 h after skin resection ( $P<0.05$ ), but there were no significant differences at 1 day after surgery (D1) and 2 days after surgery (D2). Compared with group C, the levels of MDA, IL-6, and IL-8 in group U were significantly decreased at 2 h and 4 h after skin resection ( $P<0.05$ ), and the levels of BUN and SCr in group U were significantly decreased at 1 and 2 days after skin resection ( $P<0.05$ ). Conclusion. Dexmedetomidine can effectively inhibit the release of oxygen free radicals in the shock stage and the shock recovery stage in patients with hemorrhagic trauma shock and has a protective effect on renal function.