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机构地区:[1]中南大学湘雅二医院麻醉科,长沙市410013
出 处:《中华麻醉学杂志》2009年第10期899-902,共4页Chinese Journal of Anesthesiology
基 金:国家自然科学基金资助项目(30871306)
摘 要:目的 评价异氟醚对老龄大鼠海马CA3区突触素表达的影响。方法雌性清洁级SD大鼠63只,月龄24月,体重400~650g,随机分为3组(n=21):对照组(C组)、1.2%异氟醚组(E1组)和1.8%异氟醚组(E2组)C组吸入含40%氧气的空氧混合气体3h;E1,2组吸入3%异氟醚行麻醉诱导,待翻正反射消失后再分别吸入1.2%、1.8%异氟醚维持3h。各组随机取12只大鼠,于麻醉结束后第1天采用Morris水迷宫系统测定大鼠认知功能(逃避潜伏期和探索时间),连续测定7d;随机取9只大鼠于麻醉结束后第1、3和7天处死,测定海马CA3区突触素的表达水平。结果与C组比较,E1组和E2组麻醉结束后第2、3天逃避潜伏期延长(P〈0.05或0.01),第4~6天逃避潜伏期差异无统计学意义(P〉0.05),麻醉结束后海马CA3区突触素表达持续下调(P〈0.05)。三组探索时间比较差异无统计学意义(P〉005);与E1组比较,E2组逃避潜伏期差异无统计学意义(P〉0.05),海马CA3区突触素表达下调(P〈0.01)。结论异氟醚致老龄大鼠认知功能障碍与海马突触素表达无关。Objective To investigate the effect of isoflurane on the synaptophysin expression in hippocampal CA3 area in aged rats. Methods Sixty-three 24-month-old SD rats, weighing 400-650 g, were randomly divided into 3 groups ( n = 21 each) : control group (group C) , 1.2% isoflurane group (group E1), and 1.8% isoflurane group (group E2), The rats in group C only inhaled a gas mixture containing 40% oxygen for 3 h. The rats in group E1 and E2, inhaled 3% isoflurane for induction, and after righting reflex disappeared, the concentration was reduced to 1.2% and 1.8% respectively which was maintained for 3 h. Twelve rats randomly selected from each group underwent Morris water maze test for assessment of learning and memory function (escape latency and probe time). The training test was performed 4 times a day for 7 d. Nine rats randomly selected front each group were decapitated at day 1, 3, and 7 after the termination of anesthesia. The hippocampal CA3 area was isolated for detenuination of synaptophysin expression. Results The escape latency was significantly longer at day 2 and 3 after the termination of anesthesia in group E1 and E2 than in group C ( P 〈 0.05 or 0.01 ), anti no significant difference in escape latency was found at day 4-6 after the termination of anesthesia between group E1 and E2 and group C ( P 〉 0.05). The synaptophysin expression in hippocampal CA3 area was significantly lower in grnap E1 and E2 than in group C (P 〈 0.05), and no significant difference in the probe time was found between the 3 grnups (P 〉 0.05). There was no significant difference in escape latency between group E2 and group E1 (P 〉 0.05), and the synaptophysin expression in hippocampal CA3 area was significantly lower in group E2 than in group E, ( P 〈 0.01 ) . Conclusion The cognitive dysfunction induced by isoflurane anesthesia in aged rats is not related to the synaptophysin expression in hippoeampal CA3 area.
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