Objective To investigate the effectiveness and safety of wound infiltration with rop-ivacaine for postoperative analgesia as a fast-track approach in patients undergoing open hepatectomy. Methods Fifty-two patients with hepatocellular carcinoma,32 males,20 females,aged 18-70 years, scheduled for selective open hepatectomy were enrolled in this trible-blind,randomized,controlled study.Patients were randomized to receive 0.75% ropivacaine (group ROP)or 0.9% normal saline (group NS)wound infiltration before incision closures at a total volume of 10 ml.Numerical rating score (NRS)at 6,12,24 and 48 hours after surgery,length of hospital stay,time to bowel recovery,ambulation and drainage tube extraction were recorded.Side effects, including post-operative liver and renal function,allergic reaction,nausea and vomiting,and wound infection,were also assessed.Results NRS was significantly decreased at 6 [(3.85±1.29)scores vs.(5.30±1.76) scores],12 [(3.38±0.85)scores vs.(5.69 ±1.38)scores]and 24 hours [(3.69 ±0.74)scores vs. (4.42±1.13)scores]after surgery in group ROP compared to group NS (P <0.05).Group ROP al-so showed shorter postoperative hospital stays [(1 7.92±1.97)d vs.(1 9.53±2.42)d],earlier anal exsufflation [(48.07±7.49)h vs.(53.42±10.38)h]and ambulation [(2.34±0.62)d vs.(2.80± 0.84)d](P <0.05).However,there were no significant differences between the two groups in re-garding post-operative liver and renal function.The incidence of nausea and vomiting was 1 5% (4 ca-ses)and 1 9%(5 cases)in group NS and group ROP,respectively.No allergic reactions occurred in either group.Conclusion The present study shows that ropivacaine wound infiltration could effectively release post-operative pain,and could be a safe and effective fast-track approach for patients undergoing open hepatectomy.

Objective To investigate the role and underlying mechanism of dexmedetomidine in protecting mouse neuroblastoma N2a cells against oxidative stress injury,and to discuss the effect of ERK signaling pathway.Methods Na2 cell oxidative stress injury model was established by H2O2 treatment.Cells were divided into 5 groups:control group (group C),H2O2group (group H), dexmedetomidine group (group D),H2O2+dexmedetomidine group (group HD),H2O2+dexme-detomidine+ERK inhibitor group (group HDP).Group H,group HD and group HDP were given 200 μmol/L H2O2with or without 100 ng/ml dexmedetomidine and 20 μmol/L ERK inhibitor PD98059,group D was treated with dexmedetomidine at the corresponding point,group C was treated with equal normal saline,After 1,4 hours of H2O2stimulation,cell survival,morphology changes,SOD production and ERK intracellular signaling pathway were compared between groups. Results Compared to group C,N2a cells in the group H demonstrated significantly ruduced cell sur-vival,much worse cell morphology and less SOD production (P<0.05).Compared to group H,N2a cells in group HD demonstrated significantly increased cell survival,much better preserved cell mor-phology,higher levels of SOD and enhanced ERK activation (P<0.05);Compared to group HD, cells in the group HDP had markedly decreased cell survival,worse cell morphology and lower SOD level (P<0.05).No significant changes were found in cell survival,morphology changes,SOD pro-duction and ERK intracellular signaling pathway between the groups C and D.Conclusion Dexme-detomidine protected mouse neuroblastoma N2a cells against oxidative stress injury by regulating ERK activation and SOD production.