Objective To investigate the effect of edaravone on the JAK2/STAT3 signaling pathway after ischemia-reperfusion injury in donor rat liver under different cold ischemia times. Methods A total of 102 SD rats were randomly divided into sham operation group,control group and experimental group. Six rats were in sham operation group with free liver operation and no transplantation. Forty-eight rats were in control group and experimental group respectively, and divided into subgroups according to the different cold ischemia times (30 min, 6 h, 12 h and 18 h). There were 6 donors and 6 recipients in each group. The rat model of orthotopic liver transplantation was established by modifiedtwo cuff method. All the donors were perfused by abdominal aorta and the warm ischemia time was 3-5 min. After different cold ischemia times, the experimental group was treated with edaravone (3 mg/kg) at 5 min before the opening of the new hepatic artery, and control group was injected with 3 mg/kg saline. Recipients of each group were sacrificed after 6 h. Finally, real-time fluorescence quantitative PCR was used to analyze the relative expression of JAK2/STAT3 mRNA of donor liver. Results The GAPDH gene and JAK2/STAT3 were well amplified. Under the same cold ischemia time, compared with the control group, the relative expression of JAK2/STAT3 was significantly decreased in the experimental group (P<0.05). With the prolongation of cold ischemia time, the relative expressions of JAK2 and STAT3 mRNA showed a decreasing trend in control group and experimental group, while the relative expression of JAK2 mRNA increased first and then decreased in the experimental group (P<0.05). Conclusion Edaravone has a protective effect on transplanted donor liver during different cold ischemia times, and extends the cold ischemia time for 18 h, which may be related to the inhibition of JAK2/STAT3 signal transduction pathway.

[Objective] To research the sedative effect of intranasal dexmedetomidine and sufentanil for pediatric sedation for stomatological operation of outpatient department.[Methods] 60 children undergoing stomatological operation of outpatient department,age 3 ～ 7 years,weighing 10 ～ 32 kg,of ASA physical status Ⅰ ～ Ⅱ,were divided into the three groups (n =20) randomly using a random number table:group dexmedetomidine and sufentanil (group DS),group dexmetomidine (group D),group sufentanil (group S).Recorded the children's behavior using the Ohio State University behavior rating score (OSUBRS),the University of Michigan Sedation Score (UMSS),SBP,HR and side-effects when entry,during and leave operation and in post-anesthesia care unit,side-effects,the satisfaction of stomatological doctors and parents.[Results] The OSUBRS of group DS when entry,during operation were lower than group D (P ＜ 0.01).The UMSS of group DS were higher than group D and group S when entry and during operation (P ＜ 0.05).The success rate of group DS was higher than group D and group S (P ＜ 0.01).There was no different of mean percentage change in systolic blood pressure and heart rate from baseline between group DS and group D (P ＞ 0.05).There were no instances of respiratory depression,hypotension and bradycadia.[Conclusion] Intranasal dexmedetomidine and sufentanil provides satisfactory pediatric sedation for stomatological operation of outpatient department without side effects such as respiratory depression,bradycadia and hypotension.

Objective To evaluate the effects of different administration routes of lipid emulsion on bupivacaine-induced cardiotoxicity in rats.Methods Forty-eight clean healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 6 groups (n=8 each) using a random number table:Ⅳ infusion of normal saline (NS) group (group VN),Ⅳ infusion of lipid emulsion group (group VL),duodenal infusion of NS group (group DN),duodenal infusion of lipid emulsion group (group DL),intraperitoneal intusion of NS group (group PN) and intraperitoneal infusion of lipid emulsion group (group PL).In VN and VL groups,preheated NS and 20％ lipid emulsion 3 ml · kg-1 · min-1 were infused via the femoral vein for 5 min,respectively,and then 0.75％ bupivacaine was infused at the rate of 2 mg · kg-1 · min-1 until cardiac arrest happened.Preheated NS and 20％ lipid emulsion 15 ml/kg were infused via the duodenum (over 1 min,at a constant rate) in DN and DL groups,respectively,and were intraperitoneally infused in PN and PL groups,respectively,followed by an infusion of 0.2 ml/min for 15 min in DN,DL,PN and PL groups.Then 0.75％ bupivacaine was infused via the left femoral vein at a rate of 2 mg · kg-1 · min-1 until cardiac arrest happened.The time to ventricular arrhythmia,mean arterial pressure (MAP) decreasing to 50％ of the baseline and cardiac arrest was recorded.The amount of bupivacaine consumed was calculated immediately after ventricular arrhythmia occurred (T0),immediately after MAP decreased to 50％ of the baseline (T1) and immediately after occurrence of cardiac arrest (T2).Arterial blood samples were collected at T0-2 for determination of the concentration of bupivacaine in plasma by high-performance liquid chromatography.Results Compared with group VN,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly prolonged,and the amount of bupivacaine consumed was increased at T0-2 in group VL (P＜0.01).There was no significant difference in the parameters mentioned above between group DN and group DL,and between group PN and group PL (P＞0.05).Compared with group VL,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly shortened,and the amount of bupivacaine consumed was decreased at T0-2 in DL and PL groups (P＜0.01).Compared with group DL,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly prolonged,and the amount of bupivaeaine consumed was increased at T0.2 in group PL (P＜0.05).There was no significant difference in the concentration of plasma bupivacaine between six groups (P＞0.05).Conclusion Ⅳ infusion of lipid emulsion can decrease bupivacaine-induced cardiotoxicity when compared with duodenal and intraperitoneal infusion in rats.