1-42)含量的影響。方法 隨機(jī)將120只成年SD大鼠分為七氟醚2、4、6 h組和對(duì)照組,每組30只。七氟醚2、4、6 h組分別給予3%七氟醚2、4、6 h,對(duì)照組吸入空氣。麻醉完成后1、3、7 d行Morris水迷宮實(shí)驗(yàn)和曠場(chǎng)實(shí)驗(yàn),記錄逃避潛伏期、穿越平臺(tái)次數(shù)、第3象限活動(dòng)時(shí)間、中央格停留時(shí)間、2 min穿越格子數(shù)。實(shí)驗(yàn)結(jié)束后處死大鼠取海馬組織標(biāo)本,用比色法測(cè)定AChE活性、酶聯(lián)免疫吸附試驗(yàn)測(cè)定Aβ1-42含量。結(jié)果 七氟醚組逃避潛伏期較對(duì)照組顯著延長(zhǎng)(P<0.05),第3象限活動(dòng)時(shí)間、穿越平臺(tái)次數(shù)較對(duì)照組顯著減少(P<0.05);七氟醚2、4 h組中央格停留時(shí)間、2 min內(nèi)穿越格子數(shù)與對(duì)照組無(wú)統(tǒng)計(jì)學(xué)差異,七氟醚6 h組中央格停留時(shí)間顯著大于對(duì)照組(P<0.05),2 min內(nèi)穿越格子數(shù)顯著小于對(duì)照組(P<0.05),且變化程度均與七氟醚吸入時(shí)長(zhǎng)呈正相關(guān)性。七氟醚組海馬AChE活性、Aβ1-42含量顯著高于對(duì)照組(P<0.05),且隨七氟醚吸入時(shí)間的延長(zhǎng)而升高。結(jié)論 七氟醚麻醉可導(dǎo)致大鼠認(rèn)知功能損傷,且損傷程度隨麻醉時(shí)間延長(zhǎng)而加重,其機(jī)制可能與七氟醚上調(diào)海馬AChE活性、促進(jìn)Aβ1-42生成有關(guān)。;Objective To investigate the effects of sevoflurane anesthesia time on cognitive function and acetylcholinesterase (AChE) and β-amyloid protein (Aβ1-42) 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 Aβ1-42 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 Aβ1-42 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 Aβ1-42 in hippocampus."/> 1-42"/>