Study On The Protective Mechanism Of Remifentanil On Mitochondria In Rat Hepatocytes Subjected To Ischemia-reperfusion Injury

Objective:Remifentanil, a newμ-opioid agonist with an extremely short duration of action, is metabolized by circulating and tissue esterase instead of by liver; Therefore, it is widely used as an ideal analgesic in liver operation and patients with liver dysfunction. Ischemia-reperfusion injury is the critical pathophysiological process during liver transplantation and some complex liver operations. How to reduce hepatic ischemia-reperfusion injury becomes the focus in perioperative liver protection. Intracellular calcium overload is the important mechanism of ischemia-reperfusion injury and mitochondria is the leading core associated with calcium overload, oxygen-derived free radicals and cell injury.This study is to explore the protective effect of remifentanil on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury and their possible mechanism.Materials and Methods:Sixty healthy SD rats weighting 250±20g were randomly divided into six equal groups of ten rats each: Blank group(B); Control group(C); Low remifentanil concentration group(Rl); High remifentanil concentration group(Rh); 5-HD(KATP blocker)group(HD); remifentanil+5-HD group(RHD). Rats were anesthetized with 0.5% sodium pentobarbital 40mg/kg and performed internal jugular cannulation. Rats in control group(C) were infused with saline; Rats in Rl group were infused with remifentanil 0.2 ug·kg-1·min-1; Rats in Rh group were infused with remifentanil 1 ug·kg-1·min-1; Rats in HD group were infused with 5-HD 150 ug·kg-1·min-1; Rats in RHD group were infused with remifentanil 1ug·kg-1·min-1 and 5-HD 150 ug·kg-1·min-1. After infusing for twenty minutes, the rats, abdomens were opened and the porta hepatis were clamped for thirty minutes and then declamped for one hour. Rats in blank group(B) were infused with nothing and...