目的 探讨七氟醚的麻醉时间对大鼠认知功能及海马内乙酰胆碱酯酶（AChE）活性和β-淀粉样蛋白（Aβ_1-42）含量的影响。方法 随机将120只成年SD大鼠分为七氟醚2、4、6 h组和对照组，每组30只。七氟醚2、4、6 h组分别给予3%七氟醚2、4、6 h，对照组吸入空气。麻醉完成后1、3、7 d行Morris水迷宫实验和旷场实验，记录逃避潜伏期、穿越平台次数、第3象限活动时间、中央格停留时间、2 min穿越格子数。实验结束后处死大鼠取海马组织标本，用比色法测定AChE活性、酶联免疫吸附试验测定Aβ_1-42含量。结果 七氟醚组逃避潜伏期较对照组显著延长（P<0.05），第3象限活动时间、穿越平台次数较对照组显著减少（P<0.05）；七氟醚2、4 h组中央格停留时间、2 min内穿越格子数与对照组无统计学差异，七氟醚6 h组中央格停留时间显著大于对照组（P<0.05），2 min内穿越格子数显著小于对照组（P<0.05），且变化程度均与七氟醚吸入时长呈正相关性。七氟醚组海马AChE活性、Aβ_1-42含量显著高于对照组（P<0.05），且随七氟醚吸入时间的延长而升高。结论 七氟醚麻醉可导致大鼠认知功能损伤，且损伤程度随麻醉时间延长而加重，其机制可能与七氟醚上调海马AChE活性、促进Aβ_1-42生成有关。

Objective To investigate the effects of sevoflurane anesthesia time on cognitive function and acetylcholinesterase (AChE) and β-amyloid protein (Aβ_1-42) in hippocampus of rats. Methods 120 adult SD rats were randomly divided into sevoflurane 2, 4 and 6 h groups and control group, 30 rats in each group. Sevoflurane 2, 4 and 6 h groups were given 3% sevoflurane for 2 h, 4 h and 6 h respectively, while the control group was inhaled air. Morris water maze test and open field test were performed 1, 3 and 7 days after anesthesia. The escape latency, the number of platform crossings, the activity time of the third quadrant, the residence time of the central grid and the number of grid crossings in 2 minutes were recorded. At the end of the experiment, rats were killed and hippocampal tissue samples were taken. AChE activity was measured by colorimetry, and the content of Aβ_1-42 was determined by enzyme-linked immunosorbent assay. Results The escape latency of sevoflurane experimental group was longer than that of control group (P < 0.05). The activity time of the third quadrant and the number of platform crossings were less than that of control group (P < 0.05). The escape latency decreased with the prolongation of sevoflurane inhalation time. The activity time of the third quadrant and the number of platform crossings were increased with the prolongation of sevoflurane inhalation time (P < 0.05). There was no significant difference in the residence time of the central grid and the number of grid crossings in 2 minutes between sevoflurane 2 and 4 h groups and control group. The residence time of the central grid in sevoflurane 6 h group was longer than that in control group (P < 0.05), and the number of grid crossings in 2 minutes was less than that in control group (P < 0.05). The activity of AChE and the content of Aβ_1-42 in hippocampus of sevoflurane group were higher than those of control group (P < 0.05), and increased with the prolongation of sevoflurane inhalation time. Conclusion Sevoflurane anesthesia can lead to cognitive impairment in rats, and the degree of impairment is aggravated with the prolongation of anesthesia time. The mechanism may be related to sevoflurane upregulating AChE activity and promoting the production of Aβ_1-42 in hippocampus.

R965

河南省科技发展计划项目（152300410163）