氧化应激在阻塞性睡眠呼吸暂停低通气综合征与脑梗死中的作用
发布时间：2018-07-14 21:37
【摘要】：目的：探讨氧化应激在阻塞性睡眠呼吸暂停低通气综合征（OSAHS）通过动脉粥样硬化导致脑梗死发生中的作用。 方法：按照入排标准选取研究期间住院的脑梗死患者20例、OSAHS患者20例、脑梗死+OSAHS患者20例作为病例组；在体检中心选取同一时期的健康体检者20例作为对照组。采用双抗体夹心ABC-ELISA法测定15-F2t-异前列烷的表达；采用颈动脉超声测定颈动脉内膜厚度（IMT）。 结果：（1）15-F2t-异前列烷的表达和颈动脉内膜厚度分别在对照组、脑梗死组、OSAHS组、脑梗死+OSAHS组之间进行比较差别有统计学意义（15-F2t-异前列烷：F=153.142，P0.001；IMT：F=183.056，P0.001）。（2）四组中15-F2t-异前列烷和颈动脉内膜厚度行相关分析显示在病例组中二者呈正相关，以脑梗死+OSAHS组相关性最为明显（对照组：r=-0.046，P=0.847；脑梗死组：r=0.460，P=0.041；OSAHS组：r=0.482，P=0.032；脑梗死+OSAHS组：r=0.685，P0.001）。 结论：氧化应激程度与颈动脉内膜增厚呈直线相关，在OSAHS合并脑梗死时二者明显相关，，推知OSAHS患者的氧化应激水平增高可通过诱发或加重动脉粥样硬化进而导致脑梗死发生，为临床中预防OSAHS患者发生脑梗死提供理论指导。
[Abstract]:Aim: to investigate the role of oxidative stress in cerebral infarction caused by atherosclerosis in obstructive sleep apnea hypopnea syndrome (OSAHS). Methods: 20 inpatients with OSAHS and 20 patients with OSAHS with cerebral infarction were selected as the case group according to the admission criteria, and 20 healthy persons were selected as the control group in the same period of the physical examination center. The expression of 15-F2t- isoprostaglandin was detected by double antibody sandwich ABC-ELISA, and carotid intima thickness (IMT) was measured by carotid artery ultrasound. Results: (1) the expression of 15-F2t- isoprostaglandin and carotid intima thickness were significantly different between the control group, the cerebral infarction group and the cerebral infarction OSAHS group (15-F2t- isoprostaglandin: 153.142 P 0.001). The correlation analysis of 15-F2t- isoprostaglandin and carotid intimal thickness showed that there was a positive correlation between 15 F2t- isoprostaglandin and carotid intimal thickness in four groups, especially in cerebral infarction OSAHS group (control group: 0. 046% P0. 847; cerebral infarction group: R0. 460P0. 041 OSAHS group: 0. 482P = 0. 032; cerebral infarction group: 0. 460P0. 041OSAHS group: 0. 482P0. 032; cerebral infarction group: 0. 460P0.041OSAHS group: 0. 482P0. 032) Cerebral infarction OSAHS group: 0. 685% P 0.001). Conclusion: the degree of oxidative stress is linearly correlated with carotid intima thickening, which is significantly correlated with OSAHS with cerebral infarction. It is inferred that the increase of oxidative stress level in OSAHS patients may lead to cerebral infarction by inducing or exacerbating atherosclerosis. To provide theoretical guidance for the prevention of cerebral infarction in patients with OSAHS.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R766
本文编号：2123029
[Abstract]:Aim: to investigate the role of oxidative stress in cerebral infarction caused by atherosclerosis in obstructive sleep apnea hypopnea syndrome (OSAHS). Methods: 20 inpatients with OSAHS and 20 patients with OSAHS with cerebral infarction were selected as the case group according to the admission criteria, and 20 healthy persons were selected as the control group in the same period of the physical examination center. The expression of 15-F2t- isoprostaglandin was detected by double antibody sandwich ABC-ELISA, and carotid intima thickness (IMT) was measured by carotid artery ultrasound. Results: (1) the expression of 15-F2t- isoprostaglandin and carotid intima thickness were significantly different between the control group, the cerebral infarction group and the cerebral infarction OSAHS group (15-F2t- isoprostaglandin: 153.142 P 0.001). The correlation analysis of 15-F2t- isoprostaglandin and carotid intimal thickness showed that there was a positive correlation between 15 F2t- isoprostaglandin and carotid intimal thickness in four groups, especially in cerebral infarction OSAHS group (control group: 0. 046% P0. 847; cerebral infarction group: R0. 460P0. 041 OSAHS group: 0. 482P = 0. 032; cerebral infarction group: 0. 460P0. 041OSAHS group: 0. 482P0. 032; cerebral infarction group: 0. 460P0.041OSAHS group: 0. 482P0. 032) Cerebral infarction OSAHS group: 0. 685% P 0.001). Conclusion: the degree of oxidative stress is linearly correlated with carotid intima thickening, which is significantly correlated with OSAHS with cerebral infarction. It is inferred that the increase of oxidative stress level in OSAHS patients may lead to cerebral infarction by inducing or exacerbating atherosclerosis. To provide theoretical guidance for the prevention of cerebral infarction in patients with OSAHS.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R766
【参考文献】
相关期刊论文 前3条
1 岑瑞金;;阻塞性睡眠呼吸暂停低通气综合征与脑血管病[J];重庆医学;2006年08期
2 郭乐琴;初桂兰;;在缺氧缺血性脑损伤中氧化应激时异前列烷F2a-III的作用[J];国际儿科学杂志;2006年04期
3 肖昕,熊爱华,周晓光;8-异前列腺素F_(2α):一种评估新生儿缺血性脑损伤的可靠生化指标[J];国外医学.临床生物化学与检验学分册;2005年01期
相关硕士学位论文 前3条
1 周敬;慢性间歇低氧大鼠体内氧化应激、炎症反应、内皮细胞功能障碍及N-乙酰半胱氨酸干预作用的机制研究[D];复旦大学;2009年
2 黄小玲;呼吸窘迫综合征早产儿盐酸氨溴索治疗效果及血清8-异前列素水平变化[D];暨南大学;2010年
3 梁宏伟;多巴酚丁胺负荷心血池显像对OSAHS患者心功能评价[D];山西医科大学;2010年
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