本文選題：阻塞性睡眠呼吸暫停綜合征　切入點(diǎn)：C-反應(yīng)蛋白　出處：《遵義醫(yī)學(xué)院》2012年碩士論文

【摘要】：目的：通過建立大鼠阻塞性睡眠呼吸暫停綜合征(obstructive sleep apnea syndrome, OSAS)模型及高血脂、高血糖因素參與,探討阻塞性睡眠呼吸暫停綜合征病理生理機(jī)制及其與缺血性腦卒中的相關(guān)性。 方法：Wistar大鼠隨機(jī)分為6組：正常對(duì)照組、高脂組、糖尿病組、阻塞性睡眠呼吸暫停綜合征組、阻塞性睡眠呼吸暫停綜合征+高脂組、阻塞性睡眠呼吸暫停綜合征+糖尿病組。在大鼠咽腔多點(diǎn)注射透明質(zhì)酸鈉凝膠建立OSAS模型,監(jiān)測(cè)(?)OSAS大鼠腦電圖(electroencephalogram, EEG)、口鼻氣流及動(dòng)態(tài)血氧2小時(shí),平均血氧飽和度、最低血氧飽和度及睡眠呼吸暫停指數(shù)造模前后統(tǒng)計(jì)有差異判定模型成功。①采用全自動(dòng)生化分析儀測(cè)血清C-反應(yīng)蛋白(C-reactive protein, CRP)水平,全自動(dòng)血凝儀測(cè)血漿纖維蛋白原(fibrinogen, Fbg)水平。②ELISA法測(cè)血漿同型半胱氨酸(Homocysteine,Hcy)水平。③HE染色法觀察大鼠皮質(zhì)及海馬結(jié)構(gòu)。 結(jié)果：①OSAS大鼠平均血氧飽和度(89.75±2.01)、最低血氧飽和度(72.77±5.19)降低,睡眠呼吸暫停指數(shù)(5.70±1.02)增高,與造模前比較有統(tǒng)計(jì)學(xué)差異(P0.01)。②OSAS組CRP(0.15±0.04)、Fbg(2.46±0.90)較正常對(duì)照組升高,與平均血氧飽和度成負(fù)相關(guān)(r分別為-0.802、-0.867,P0.01),與睡眠呼吸暫停指數(shù)成正相關(guān)(r分別為0.874、0.941,P0.05)；OSAS+高脂組大鼠CRP(0.15±0.04)、Fbg(2.78±1.50)較正常對(duì)照組升高,與平均血氧飽和度成負(fù)相關(guān)(r分別為-0.901、-0.963,P0.05),與睡眠呼吸暫停指數(shù)成正相關(guān)(r分別為0.933、0.975,P0.05)；OSAS+糖尿病組大鼠CRP(0.16±0.03)、Fbg(3.27±1.83)較正常對(duì)照組升高,與平均血氧飽和度成負(fù)相關(guān)(r分別為-0.881、-0.869,P0.05),與睡眠呼吸暫停指數(shù)成正相關(guān)(r分別為0.928、0.990,P0.05)。③OSAS+高脂組大鼠Hcy(10.94±2.48)水平較其它五組增高,差異有統(tǒng)計(jì)學(xué)意義(P0.05),與睡眠呼吸暫停指數(shù)成正相關(guān)(r為0.867,P0.05)。④OSAS組大鼠腦組織HE染色皮質(zhì)及海馬區(qū)有神經(jīng)元缺失、排列紊亂及腦小血管增生,OSAS+高脂組、OSAS+糖尿病組較OSAS組改變明顯。 結(jié)論：①OSAS大鼠CRP、Fbg、Hcy水平升高,與OSAS病情程度密切相關(guān)。OSAS大鼠炎癥反應(yīng)增強(qiáng)、血液高凝狀態(tài)、高同型半胱氨酸血癥,可能是OSAS發(fā)生缺血性腦卒中的發(fā)病機(jī)制。②OSAS大鼠皮質(zhì)及海馬區(qū)有神經(jīng)元缺失、排列紊亂及腦小血管增生表現(xiàn)。
[Abstract]:Objective: to investigate the pathophysiological mechanism of obstructive sleep apnea syndrome (OSASs) and its correlation with ischemic stroke by establishing a rat model of obstructive sleep apnea syndrome (OSASs) and the involvement of hyperlipidemia and hyperglycemia. Methods Wistar rats were randomly divided into 6 groups: normal control group, hyperlipidemia group, diabetes group, obstructive sleep apnea syndrome group, obstructive sleep apnea syndrome hyperlipidemia group. OSAS model was established by injecting sodium hyaluronate gel into the pharyngeal cavity of rats with obstructive sleep apnea syndrome diabetes mellitus. OSAS rats electroencephalograms, EEGG, oral and nasal airflow and dynamic oxygen for 2 hours, mean oxygen saturation, The statistical difference between the lowest oxygen saturation and sleep apnea index before and after the establishment of the model. 1 the serum level of C-reactive protein (CRPP) was measured by automatic biochemical analyzer. The plasma fibrinogen fibrinogen (Fbg) level was measured by automatic hemagglutination instrument. 2The plasma homocysteine homocysteine homocysteine (HcyH) level was measured by Elisa. 3 he staining was used to observe the structure of cortex and hippocampus in rats. Results the mean blood oxygen saturation and the lowest oxygen saturation were decreased, and the sleep apnea index was 5.70 鹵1.02). Compared with the control group, there was significant difference between the two groups (P < 0.01). The mean oxygen saturation (CRP(0.15) in the control group was 2.46 鹵0.90), which was higher than that in the normal control group (P < 0.01), and was significantly higher than that in the control group (P < 0.01), and was significantly higher than that in the normal control group (P < 0.05), and the sleep apnea index was 5.70 鹵1.02 (P < 0.05). The negative correlation with the mean oxygen saturation was -0.802- 0.867U P0.01g, and the positive correlation with the sleep apnea index was 0.874U 0.941P0.05OSAS in the hyperlipidemic rats, CRP(0.15 鹵0.04 FBG 2.78 鹵1.50 was higher than that in the normal control group. The negative correlation with the mean oxygen saturation was -0.901U -0.963U P0.05A, and the positive correlation with the sleep apnea index was 0.933 鹵0.975P0.05. the CRP(0.16 of the diabetic rats in the diabetic group was higher than that in the normal control group (3.27 鹵1.83). The negative correlation with the mean oxygen saturation was -0.881- 0.869U P0.05A, and the positive correlation with the sleep apnea index was 0.928890g P0.05P0.05.3OSAS, the level of Hcy(10.94 鹵2.48in the hyperlipidemia group was higher than that in the other five groups. The difference was statistically significant (P 0.05), and the positive correlation with the sleep apnea index was 0. 867 (P 0. 05) P 0. 05. 4OSAS. There were neuronal deletions in the cortex and hippocampus of the rats in the HE staining group. The changes of neurons in the hyperlipidemic group were significantly different from those in the OSAS group. Conclusion the level of FbgCy in CRP1OSAS rats is increased, which is closely related to the severity of OSAS. The inflammatory response is increased, blood hypercoagulability and hyperhomocysteinemia are observed in OSAS rats. It may be the pathogenesis of ischemic stroke in OSAS. There are neuronal deletion, disarrangement and small vascular hyperplasia in cortex and hippocampus of OSAS rats.
【學(xué)位授予單位】：遵義醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R766;R743.3

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本文編號(hào)：1668253