目的 研究地塞米松预处理对长时程异氟醚麻醉后认知功能的影响。 方法 将32只C57BL/6小鼠按随机数字表法分为对照组（C组，8只）、麻醉组（A组，9只）、地塞米松组（D组，8只）和地塞米松+麻醉组（DA组，7只）。D组和DA组小鼠预先给予连续7 d地塞米松5 mg·kg-1·d-1腹腔注射后，A组和DA组小鼠行长时程异氟醚麻醉，异氟醚浓度为1.0%~1.5%，麻醉时长6 h。麻醉后14 d内检测小鼠空间记忆能力和情景记忆能力。各组小鼠于麻醉后1、3、7、14 d取右侧海马采用实时荧光定量PCR法检测糖皮质激素受体（glucocorticoid receptor, GR）和N-甲基-D-天门冬氨酸受体2B（N-methyl-D-aspartate receptor subunit 2B, NR2B） mRNA的表达情况。 结果 A组小鼠在异氟醚麻醉后2~11 d，正确象限访问率下降（P＜0.05）。麻醉后第3、7天，A组小鼠辨别指数（discrimination index, DI）均分别低于C组、DA组，差异有统计学意义（P＜0.05）。异氟醚麻醉后1、3、7 d，A组小鼠海马区NR2B mRNA水平比C组均增加（P＜0.05），预给予地塞米松后上调麻醉后NR2B mRNA表达水平的降低（P＜0.05）。 结论 长时程异氟醚麻醉可引起小鼠空间记忆能力和情景记忆能力的损伤，而预给予地塞米松可改善这一损伤效应，GR和NR2B介导的信号通路可能参与其中。
Ｏｂｊｅｃｔｉｖｅ To observe the effect of dexamethasone on cognition after long-term isoflurane anesthesia. Methods Used C57BL/6 mice were randomly divided into 4 groups: control group(group C), anesthesia group(group A), dexamethasone group(group D) and dexamethasone pretreatment plus anesthesia group(group DA). Mice in group D and group DA were administrated intraperitoneally of dexamethasone at a dose of 5 mg/kg for consecutive 7 days. Mice in group A and group DA were anesthetized by isoflurane for 6 h at a concentration of 1.0%-1.5%. Space memory and contextual memory of mice were tested at day 14. Results In our study, we found that the mice in group A showed remarkable space memory impairment from day 2 to day 11(P<0.05), and dexamethasone pretreatment can reverse this effect(P<0.05). In addition, mice in group A showed more remarkable contextual memory impairment than contextual memory in group C(P＜0.05) and group DA(P＜0.05) at day 3. Mice in group A also showed more remarkable contextual memory impairment than memory impairment in group C(P＜0.05) and group DA(P＜0.05) at day 7. In addition, the relative mRNA level of N-methyl-D-aspartate receptor subunit 2B(NR2B) in group A decreased compared to group C, but dexamethasone pretreatment can prevent the decrease of NR2B mRNA from day 1 to day 7(P＜0.05). Conclusions Long-term isoflurane anesthesia can impair space memory and contextual memory in mice which can be reversed by dexamethasone pretreatment, and glucocorticoid receptor(GR) and NR2B signal pathway may be involved in it.
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