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作 者:李艳[1] 聂秀红[1] 张威[1] 樊晓军[1] 任魁[1] 高赏[1]
机构地区:[1]首都医科大学宣武医院呼吸科,北京100053
出 处:《首都医科大学学报》2013年第4期609-614,共6页Journal of Capital Medical University
摘 要:目的探讨不同程度阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)患者体内植物凝集素样氧化低密度脂蛋白受体-1(lectin-like oxidized low-density lipoprotein receptor-1,LOX-1)的水平及氧化应激对其影响。方法根据睡眠呼吸暂停低通气指数(apnea-hypopnea index,AHI)将2011年1月至2011年7月来自宣武医院呼吸科门诊就医患者94例分为3组,分别是轻中度组29例,重度组35例,对照组30例,各组均于多导睡眠图监测后检测血清LOX-1、氧化低密度脂蛋白(oxidized low-density lipoprotein,ox-LDL)、丙二醛(malondialdehyde,MDA)浓度。结果重度OSAHS组血清LOX-1、oxLDL、MDA浓度最高,轻中度组、对照组依次减低,差异有统计学意义(P<0.01)。OSAHS患者血清LOX-1浓度与血清ox-LDL和MDA浓度呈正相关(r值分别为0.693、0.460,P<0.01)。ox-LDL和夜间最低血氧饱和度(minimal satuation of blood oxygen,SaO2min)浓度是影响OSAHS患者血清LOX-1的独立危险因素(r值分别为0.705,0.734,P<0.01)。结论 OSAHS所造成的夜间间歇缺氧可通过氧化应激途径调节LOX-1水平,进一步促成OSAHS患者动脉粥样硬化病变的形成和发展。Objective To investigate the changes of serum lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and the influence from oxidative stress in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). Methods Totally 94 candidates were divided into three groups according to the apnea-hypopnea index( AHI), including normal control group( n = 30), mild to moderate group( n = 29 ), severe group( n = 35 ). After the monitoring by polysomnography( PSG), the blood samples were obtained to measure the levels of serum LOX-1, oxidized low-density lipoprotein(ox-LDL) and malondialdehyde(MDA). Results The levels of serum LOX-1, ox-LDL, MDA in severe OSAHS group were significantly higher than that in the mild to moderate group and control group( P〈0.01 ). The level of serum LOX-1 in OSAHS patients was positively correlated with serum ox-LDL and MDA(r=0. 693, 0.460, respectively, all P〈 0.01 ). The level of ox-LDL and SaO2min were the high risk factors to influence the level of serum LOX-1 in patients with OSAHS(r= 0. 705, 0.734, respectively, all P〈0.01 ). Condusion The intermittent hypoxia caused by OSAHS can regulate the levels of LOX-1 through oxidative stress, and can further promote the formation and develooment of atherosclerotic in oatients with OSAHS.
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