本文關(guān)鍵詞： 間歇性低氧 阻塞性睡眠呼吸暫停低通氣綜合征 學(xué)習(xí)記憶功能 海馬超微結(jié)構(gòu) 水迷宮　出處：《華北煤炭醫(yī)學(xué)院》2010年碩士論文　論文類型：學(xué)位論文

【摘要】：目的: 通過模擬OSAHS的發(fā)病特征,建立大鼠間歇性低氧(IH)模型,觀察5%間歇低氧條件下,不同暴露時(shí)間過程對(duì)大鼠的學(xué)習(xí)記憶功能的影響和海馬CA1區(qū)超微結(jié)構(gòu)的改變,為研究OSAHS引起的認(rèn)知功能損害提供實(shí)驗(yàn)基礎(chǔ)。 方法: 選擇成年雄性Wistar大鼠(體重約170±10g)48只,隨機(jī)均分為2組:空白對(duì)照組(UC組)和5%間歇性低氧組(5%IH組),UC組放入艙內(nèi)給予壓縮空氣,IH組大鼠每日放入自制的低氧艙內(nèi)暴露8小時(shí),分別暴露2、4、6、8周。各組大鼠均常規(guī)飼養(yǎng)。在實(shí)驗(yàn)結(jié)束后進(jìn)行Morris水迷宮實(shí)驗(yàn);利用光鏡和電鏡觀察海馬組織結(jié)構(gòu)和超微結(jié)構(gòu)的變化。 結(jié)果: 1、Morris水迷宮測(cè)試成績(jī):①定位航行實(shí)驗(yàn):各組大鼠的逃避潛伏期均隨實(shí)驗(yàn)天數(shù)延長(zhǎng)而逐漸縮短,不同天數(shù)之間比較,逃避潛伏期有明顯差異(P0.05)。IH各組逃避潛伏期隨著缺氧時(shí)間延長(zhǎng)呈逐漸延長(zhǎng)趨勢(shì)。不同暴露組之間及與對(duì)照組的逃避潛伏期比較不完全相同。5%IH2周組與6周、8周組比較,4周組與8周組比較差異顯著(P0.05),其它各組內(nèi)比較無差異明顯(P0.05)。②Morris水迷宮記憶成績(jī):⒈跨越目標(biāo)象限時(shí)間:各CIH組隨著低氧時(shí)間延長(zhǎng)和低氧濃度的降低,跨越目標(biāo)象限時(shí)間呈逐漸縮短趨勢(shì)。IH組與UC組之間比較有顯著差別(P0.05)。5%CIH2周組和4、6、8周組比較差異顯著(P0.05);⒉穿臺(tái)次數(shù):采用非參數(shù)檢驗(yàn)(秩和檢驗(yàn)),不同暴露條件之間以及不同暴露時(shí)間之間不完全相同,隨著間歇低氧濃度的降低,穿臺(tái)次數(shù)減少,P0.01。 2、光鏡下海馬組織結(jié)構(gòu)的變化 隨著間歇低氧時(shí)間的延長(zhǎng),早期表現(xiàn)為核固縮呈強(qiáng)嗜堿性,核染色質(zhì)聚集在核膜下呈環(huán)狀,晚期凋亡表現(xiàn)為核溶解碎裂等,尼氏體結(jié)構(gòu)逐漸變模糊并發(fā)生崩解。隨著暴露時(shí)間的延長(zhǎng)神經(jīng)元數(shù)量減少。亦可見腫脹神經(jīng)元細(xì)胞,表現(xiàn)為細(xì)胞空泡化,透亮度增高,胞漿成分不明顯。3、電鏡觀察可見正常海馬神經(jīng)元核核大而圓,核仁清晰,核質(zhì)均勻散在,核膜光滑,邊緣清晰,細(xì)胞器豐富完整。間歇低氧組隨著暴露時(shí)間的延長(zhǎng),海馬神經(jīng)元早期表現(xiàn)為細(xì)胞核形態(tài)變化不明顯,糖原顆粒減少。后期出現(xiàn)核溝,并逐漸加深加大,染色質(zhì)邊集。細(xì)胞器逐漸減少,線粒體空泡化并出現(xiàn)異型結(jié)構(gòu),粗面內(nèi)質(zhì)網(wǎng)表面的脫顆�，F(xiàn)象逐漸加重。神經(jīng)元數(shù)量減少。突觸結(jié)構(gòu)隨暴露時(shí)間逐漸出現(xiàn)突觸小泡增大,結(jié)構(gòu)模糊,突觸間隙增寬。暴露至6周時(shí)脫髓鞘現(xiàn)象達(dá)高峰。各時(shí)間段血管均有不同程度的水腫。 結(jié)論: 1、間歇性低氧可造成大鼠學(xué)習(xí)記憶功能的降低。隨著暴露時(shí)間的延長(zhǎng),大鼠學(xué)習(xí)記憶功能損害呈現(xiàn)逐漸加重趨勢(shì),慢性間歇性低氧在暴露一定時(shí)間后出現(xiàn)明顯的學(xué)習(xí)記憶功能障礙。 2、間歇性低氧可引起海馬神經(jīng)元的損害,隨著暴露時(shí)間的延長(zhǎng)而逐漸加重。
[Abstract]:Objective:. The intermittent hypoxic OSAHS model was established by simulating the pathogenesis of OSAHS in rats. The effects of 5% intermittent hypoxia on the learning and memory function of rats and the ultrastructure of hippocampal CA1 were observed. To provide experimental basis for the study of cognitive impairment induced by OSAHS. Methods:. 48 adult male Wistar rats (weight about 170 鹵10g / g) were randomly divided into two groups: control group (UUC group) and 5% intermittent hypoxia group. Rats in the 5% intermittent hypoxia group were exposed to hypoxia for 8 hours daily. At the end of the experiment, the Morris water maze test was carried out, and the changes of hippocampal tissue structure and ultrastructure were observed by light and electron microscopy. Results:. (1) Morris water maze test score of 1: 1 navigation experiment: the escape latency of rats in each group was shortened with the prolongation of experimental days, and was compared among different days. There was a significant difference in escape latency between P0.05 and IH groups with the prolongation of hypoxic time. The escape latency of different exposure groups and control group was not exactly the same. 5IH2 week group and 6-week 8 week group were different. There was significant difference between the 4th week group and the 8-week group (P 0.05), but there was no significant difference in the other groups. The memory score of the water maze: 1: 1 crossed the target quadrant time: each CIH group with the increase of hypoxic time and the decrease of hypoxic concentration. The time of crossing the target quadrant was gradually shortened. There was significant difference between IH group and UC group. There were significant differences between the two groups (P0.05N. 5CIH _ 2 week group and 4o 66-week group). The number of platform penetration was significant (P 0.05): nonparametric test was used (rank sum test, different exposure conditions were compared with each other). And different exposure times, With the decrease of intermittent hypoxia concentration, the number of table penetration decreased (P 0.01). 2. Changes of hippocampal tissue structure under light microscope. With the prolongation of intermittent hypoxic time, nuclear pyknosis appeared as strong basophilic in the early stage, nuclear chromatin gathered under the nuclear membrane in the annular shape, and late apoptosis appeared as nuclear dissolution and fragmentation, etc. The structure of Nissl's body gradually became blurred and disintegrated. The number of neurons decreased with the prolongation of exposure time. The cytoplasmic components were not obvious. The electron microscopic observation showed that the nucleus of normal hippocampal neurons was large and round, the nucleoli were clear, the nucleus was evenly dispersed, the nuclear membrane was smooth, the edge was clear, and the organelle was abundant and complete. In the early stage of hippocampal neurons, the nuclear morphology was not obvious, the glycogen granules were decreased, the nuclear sulcus appeared in the later stage, the chromatin side set was gradually increased, the organelle was gradually decreased, the mitochondria vacuolated and appeared abnormal structure. The degranulation of rough endoplasmic reticulum (ER) surface was gradually aggravated, and the number of neurons decreased. The synaptic vesicles gradually increased with the exposure time, and the structure of synaptic vesicles was blurred. The demyelinating phenomenon reached its peak after 6 weeks of exposure, and the blood vessels showed various degrees of edema at each time point. Conclusion:. 1. Intermittent hypoxia induced the decrease of learning and memory function in rats. With the prolongation of exposure time, the impairment of learning and memory in rats showed a tendency to aggravate gradually. Chronic intermittent hypoxia after a certain period of exposure to significant learning and memory impairment. 2. Intermittent hypoxia may cause damage to hippocampal neurons, which is aggravated with the prolongation of exposure time.
【學(xué)位授予單位】：華北煤炭醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R363

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