背景妨碍的睡觉呼吸暂停症候群(OSAS ) 是为心血管的疾病的一个重要风险因素。长期的断断续续的组织缺氧(CIH ) 被认为是在 OSA 病人的心血管的疾病的最重要的原因之一。这个重复组织缺氧和氧化周期类似于 hypoxia-reperfusion 损害,它开始氧化应力。在这研究,我们观察了 CIH 和 N-acetylcysteine (NAC ) 的效果导致的 cardiocytes 损害。三十只 ICR 老鼠随机被分到 3 个组的方法:控制, CIH 和 NAC (CIH+NAC ) 组。Malondialdehyde (MDA ) 和 cardiocyte homogenates 的 superoxide dismutase (草皮) 被测量。浆液类脂化合物被一个仪器方法测量。浆液心脏的 troponin (cTnl ) 我被连接酶的 immunosorbent 试金(ELISA ) 检测。心肌层病理学的节是草皮活动和在 CIH 的 cardiocyte homogenates 的 MDA 集中组织的 observed.Results (1 ) 比在另外的组显著地高(P < 0.005 ) 。NAC 组的 MDA 集中比控制组的低(P < 0.01 ) 。(2 ) CIH 和 NAC 组的浆液 cTnl 集中比控制组的显著地高(P < 0.01 ) 。(3 ) 在 NAC 组的浆液 triglyceride 层次比在另外的组低(P < 0.01 ) ,当在低密度脂蛋白和高密度没有重要差别时,在三之中的脂蛋白组织。(4 ) 心肌层,模糊的横向的有条纹或刻痕之状态,和织物流出的退化在 CIH 和 NAC 组在织物节被观察。然而,正常织物在 CIH 导致的氧化压力能伤害的控制 group.Conclusion 被发现 cardiocytes 和损害效果罐头被 NAC 部分禁止。
Background Obstructive sleep apnea syndrome (OSAS) is an important risk factor for cardiovascular diseases. Chronic intermittent hypoxia (CIH) is considered to be one of the most important causes of cardiovascular diseases in OSA patients. This repeated hypoxia and reoxygenation cycle is similar to hypoxia-reperfusion injury, which initiates oxidative stress. In this study, we observed cardiocytes injury induced by CIH and the effect of N-acetylcysteine (NAC). Methods Thirty ICR mice were randomly assigned to 3 groups: control, CIH and NAC (CIH+NAC) groups. Malondialdehyde (MDA) and superoxide dismutase (SOD) of cardiocyte homogenates were measured. Serum lipids were measured by an instrument method. Serum cardiac troponin I (cTnl) was detected by enzyme-linked immunosorbent assays (ELISA). Myocardium pathological sections were observed. Results (1) The SOD activity and MDA concentration of cardiocyte homogenates in the CIH group were significantly higher than in other groups (P 〈0.005). The MDA concentration of the NAC group was lower than that of the control group (P 〈0.01). (2) The serum cTnl concentration of the CIH and NAC groups was significantly higher than that of the control group (P 〈0.01). (3) Serum triglyceride levels in the NAC group were lower than in the other groups (P 〈0.01), while there were no significant differences in low density lipoprotein and high density lipoprotein among the three groups. (4) The degeneration of myocardium, transverse striation blurred, and fabric effusion were observed in tissue sections in the CIH and NAC groups. However, normal tissue was found in the control group. Conclusion The oxidative stress induced by CIH can injure cardiocytes and the injury effect can be partially inhibited by NAC.