ABSTRACT
Objective To evaluate the effect of dexmedetomidine on the expression of brain-derived neurotrophic factor (BDNF) during lidocaine-induced spinal neurotoxicity in rats.Methods Fifty-six male Sprague-Dawley rats,weighing 250-280 g,aged 2-3 months,were divided into 7 groups (n =8 each) using a random number table:sham operation group (group S),lidocaine group (group L),normal saline group (group NS),3 different doses of dexmedetomidine groups (D1,D2 and D3 groups),and oα2-adrenoceptor antagonist yohimbine group (group Y).An epidural catheter was placed at L5.6 interspace.Ten percent lidocaine 20 μl was injected intrathecally in all groups except group S.Dexmedetomidine 5,15 and 25 μg/kg were injected intraperitoneally at 30 min before lidocaine injection in D1,D2 and D3 groups,respectively.In group Y,yohimbine 1.0 mg/kg was injected intraperitoneally at 15 min before dexmedetomidine 25 μg/kg was injected.Before intrathecal administration and at 24,48 and 72 h after intrathecal administration (T1-4),the Basso,Beattie,Bresnahan (BBB) Locomotor Rating Scale was used,and the tail flick latency to a thermal nociceptive stimulus (TFL) was measured to assess the locomotor function.The rats were sacrificed after the last behavioral test,and the lumbar segments (L3-5) of the spinal cord were removed for pathological examination and for determination of BDNF expression and cell apoptosis.The apoptosis index was calculated.Results Compared with group S,the BBB score was significantly decreased at T2-4,the TFL was prolonged,the BDNF expression was up-regulated,and apoptosis index was increased in L,NS,D1,D2 and D3 groups (P＜0.05).Compared with group L,the BBB score was significantly increased at T2-4,the TFL was shortened,the BDNF expression was up-regulated,and apoptosis index was decreased in group D3 (P＜0.05),and no significant change was found in the parameters mentioned above in NS,D1,D2 and Y groups (P＞0.05).Compared with group D3,the BBB score was significantly decreased at T2 4,the TFL was prolonged,the BDNF expression was down-regulated,and apoptosis index was increased in group Y (P＜0.05).The pathological changes of the spinal cord were significantly attenuated in group D3 as compared with group L,and there was no significant difference in pathological changes of the spinal cord between group Y and group L.Conclusion The mechanism by which dexmedetomidine reduces lidocaine-induced spinal neurotoxicity may be related to up-regulation of BDNF expression,and the mechanism by which dexmedetomidine up-regulates BDNF expression is completely related to activation of α2-adrenoceptors in rats.
ABSTRACT
Objective To determine the minimum alveolar concentration (MAC) of sevoflurane in Chinese neonates.Methods Thirty ASA Ⅰ or Ⅱ neonates,aged ≤ 28 days,with normal body weight,scheduled for elective surgery under general anesthesia,were enrolled in the study.Anesthesia was induced with inhalation of 6.00％ sevoflurane in oxygen.The infants were tracheal intubated and mechanically ventilated.The inhaled concentration of sevoflurane was adjusted to achieve the preset end-tidal concentration and maintained at this level for 20 min.Skin incision was then performed.The concentration of sevoflurane was determined by modified Dixon's up-and-down method.The initial end-tidal concentration of sevofluren was 3.00％.Each time the concentration increased/decreased by 0.25 ％ in the next infant according to the infant's response.Successful skin incision was defined as no body movement during skin incision.The MAC,ED95 and 95 ％ confidence interval of sevoflurane were calculated using logistic regression analysis.Results The MAC and ED95 (95 ％ confidence interval) of sevoflurane required for successful skin incision were 2.82％ (2.66％-2.98％) and 3.39％ (2.89％-3.89％),respectively,in neonates.Conclusion The MAC of sevoflurane is 2.82 ％ in Chinese neonates and lower than the present reference values previously described in foreign reports.