To investigate the effect of dexmedetomidine on digestive functions after hepatectomy in patients with liver cirrhosis under general anesthesia.

In this prospective, randomized, double-blind investigation, fifty patients with liver cirrhosis undergoing elective hepatectomy were randomized into dexmedetomidine group and control group. General anesthesia was conducted with a target-controlled infusion of propofol at a plasma target concentration of 3-4 μg/ml, 3 μg/kg fentanyl, and 0.2 mg/kg cisatracurium. After tracheal intubation, anesthesia was maintained with a target-controlled infusion of propofol, remifentanil 0.1-0.3 μg·kg^-1·min^-1, and cisatracurium 5-10 mg boluses according to clinical needs. The dexmedetomidine group received a loading dose of 1 μg/kg dexmedetomidine over 15 min right after the intubation, then followed by a maintenance dose of 0.3 μg·kg^-1·h^-1 to the end of operation. In the control group, 0.9% sodium chloride was administered. Venous blood was collected at five time points: baseline (before surgery), 1, 6, 24, and 72 h after hepatectomy. The observation targets included the variables reflecting (1) intestinal injury: serum diamine oxidase (DAO) and D-lactic acid (LAC); (2) liver function: AST and ALT; (3) inflammatory response: TNF-α and IL-6; (4) oxidative stress: MDA.

DAO activity and D-LAC levels were lower in the dexmedetomidine group than in the control group after liver reperfusion (P<0.05). Also, the biomarkers reflecting liver injury increased over time, but were lower in the dexmedetomidine group (P<0.05). And the variables reflecting inflammatory response and oxidative stress were lower in the dexmedetomidine group than in the control group after liver reperfusion (P<0.01).

Dexmedetomidine administered perioperatively attenuates intestinal and hepatic injury in patients with liver cirrhosis after hepatectomy under general anesthesia. The protective mechanism of dexmedetomidine against intestinal and hepatic injury has a close relationship with inhibition of systemic inflammatory response and oxidant stress.