Objective: To compare the anesthetic and analgesic efficacy of ropivacaine and bupivacaine and their side reactions in combined spinal epidural anesthesia (CSEA) and postoperative analgesia in pediatric surgery. Methods: Fifty children for lower abdominal surgery, aged 6-14 years, were randomly assigned to receive either ropivacaine (Group R, n =25) or bupivacaine (Group B, n =25) for CSEA. Spinal injection for Group R was a mixture of 1.5 ml of 10 g?L -1 ropivacaine, 0.5 ml distilled water and 1ml of 100 g?L -1 dextrose. The injection for Group B was the same as that for Group R except 0.5 ml of 7.5 g?L -1 bupivacaine . The terminal concentrations of anesthetics were 5 g?L -1 for the two groups. The injection volume was calculated as: ml=(age?0.2+weight?0.5)/2. When operations prolonged to 1.5 h, epidural infusion at the rate of 1 mg?kg -1 ?h -1 started with 2.5 g?L -1 ropivacaine for Group R and 2.5 g?L -1 bupivacaine for Group B. The observed variables were the changes in blood pressure, heart rate, SpO 2, block level, visual analogue scores, and motor block. Epidural postoperative analgesia was performed for Group R with 100 ml of 0.75 g?L -1 ropivacaine to which 100 mg tramadol and 5 mg were added, and for Group B with 100 ml of 0.75 g?L -1 bupivacaine instead. Backgroup infusion was 3 ml?h -1 for the children aged 6-9 years or 4 ml?h -1 for the children aged 10-14 years, bolus was 2 ml controlled by children or their parents when necessary, and locktime was 15 min. The observed variables were the efficacy of postoperative analgesia, recession of motor block of legs, and the incidence of headache, nausea and vomiting, leg numbness, and urinary retention within 24 h after operation. Results: There was no significant difference between the two groups in block level. Motor block was much milder in Group R than that in Group B during operation, and recessed faster after operation. Only one case of nausea occurred in each group, and one case of urinary retention in Group B without statistical significance. Conclusion: Either ropivacaine or bupivacaine can be satisfactorily used in CSEA for analgesia during and after operation. However, ropivacaine has a weaker motor block than bupivacaine, which benefits early walking after operation and recovery of bowl movement.

Objective To study the influence of GM1 on hyperbilirubinemia-induced brain injury in neonatal rats and its possible mechanism.Method A total of 120 7-day-old Sprague-Dawley (SD) rats were randomly assigned into normal control group (n =40),hyperbilirubinemia group (n =40) and GM1 group (n =40).According to the different duration of hyperbilirubinemia,each group was further assigned into 5 subgroups,6 h,12 h,24 h,48 h and 72 h group (n =8).The model of neonatal rat with hyperbilirubinemia was established injecting bilirubin solution (100 μg/g) intraperitoneally.GM1 (10 mg/kg) was injected intraperitoneally immediately after the model was established in GM1 group.Immunohistochemical method was used to determine the expression of Bax in hippocampus.TUNEL method was used to measure the neural cell apoptosis index (AI) in the brain.Result Six hours after the hyperbilirubinemia model was set up,the expression of Bax and AI in hyperbilirubinemia group and GM1 group were examined.The median of AI were 33.5％ and 15.4％ respectively and the average grey value of Bax positive cells were 157.4 ± 2.8 and 162.9 ± 2.3.Both apoptosis cells and the expression of Bax were gradually increasing,and peaked at 72 h after the model was established.The median of AI were 55.5％ and 35.5％ respectively,and the average grey value of Bax positive cells were 127.8 ± 3.6 and 141.5 ±2.7 in hyperbilirubinemia group and GM1 group.And the expressions of Bax and AI in the control group were nearly undetectable.The expression of Bax and AI in GM1 group were lower than hyperbilirubinemia group,but higher than the control group,the differences were statistically significant (P ＜ 0.001).Conclusion Brain cells apoptosis is influenced by hyperbilirubinemia-induced brain injury and Bax may be involved in the process.GM1 may reduce the brain damage by inhibiting the expression of Bax to reduce the apoptosis of the brain cells.