Effects of remifentanil preconditioning on intestinal ischemia-reperfusion injury in rats：the rela-tionship with opioid receptors / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of remifentanil preconditioning ( RP ) on intestinal is?chemia?reperfusion ( I∕R) injury in rats and its relationship with opioid receptors. Methods Seventy?two Sprague?Dawley rats, aged 6-7 weeks, weighing 250-280 g, were randomly divided to 9 groups ( n=8 each) sham operation group (S), intestinal I∕R group (group I∕R), RP group, different opioid receptor antagonists groups (N, BNI and CTOP groups), and opioid receptor antagonists + RP groups (N+RP, BNI+RP and CTOP+RP groups) . Intestinal I∕R was produced by clamping the superior mesenteric artery for 1 h followed by 2 h reperfusion in all the groups except group S. RP was induced by 3 cycles of 5 min infusion of remifentanil 0?2 μg·kg-1 ·min -1 followed by 5 min infusion of normal saline before ischemia. Naltrindole (δ?receptor antagonist, 5 mg∕kg) , nor?binaltorphimine (κ?receptor antagonist, 5 mg∕kg) and CTOP (μ?receptor antagonist, 1 mg∕kg) were administered before RP. At 2 h of reperfusion, blood sam?ples were collected from the cardiac apex for determination of serum diamine oxidase ( DAO) activity. Intes? tinal tissues were then removed for microscopic examination. Intestinal damage was assessed and scored ac?cording to Chiu. Apoptosis in intestinal mucosal epithelial cells was detected using TUNEL assay, and ap?optosis index was calculated. The expression of activated caspase?3 in intestinal mucosal epithelial cells was measured by Western blot. Results Compared with group S, the serum DAO activity, Chiu′s score, and apoptosis index were significantly increased, and the expression of activated caspase?3 was up?regulated in I∕R and RP groups ( P0?05). Compared with group RP, the serum DAO activity, Chiu′s score, and apoptosis index were significantly increased, and the expression of activa?ted caspase?3 was up?regulated in N+RP and CTOP+RP groups ( P0?05) . Conclusion RP can mitigate in?testinal I∕R injury in rats, and the mechanism is related to the anti?apoptotic effect mediated by activation ofδ?and μ?opioid receptors, but not κ?opioid receptors.