Increased adiposity does not exacerbate impaired vasodilation in rats exposed to eucapnic intermittent hypoxia.
Increased adiposity does not exacerbate impaired vasodilation in rats exposed to eucapnic intermittent hypoxia.
复制标题
暴露于常碳酸间歇性缺氧的大鼠中，肥胖增加不会加剧血管舒张受损。
DOI：
10.1159/000320322
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Walker,BenjimenR
中科院分区：
文献类型：
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作者：
Sweazea,KarenL;Kanagy,NancyL;Walker,BenjimenR
BackgroundAlthough有经常是增加肥胖症和阻塞性睡眠呼吸暂停的临床并发症，每个因素都独立地与升高的氧化应激。我们假设，超重大鼠暴露于模拟的睡眠呼吸暂停将开发加剧氧化应激导致受损的内皮依赖vasodilation.MethodsRats被喂以食物或高脂饮食（HFD; 60%千卡脂肪）6周。在每种饮食的最后14天，动物暴露于空气或eucapnic间歇性缺氧（E-IH），以模拟睡眠apnea.ResultsRats暴露于E-IH或HFD单独显示增加161和176%，分别在氧化应激（硫代巴比妥酸反应物质测量）相比，食物+空气控制。然而，与每个单独的处理相比，在组合的HFD+ E-IH处理（食物+空气对照的132%）后氧化应激较低。所有三个治疗组，食物+ E-IH，HFD+空气和HFD+ E-IH，（分别为144.5±4.4、148.2±5.6和136.2±2.0 mm Hg，与食物+空气相比：123±2.0 mm Hg）和减弱乙酰胆碱（ACh）介导的血管舒张（78.3，72.7，和78.2%的食物+空气反应在最高剂量的乙酰胆碱）相比，食物+空气对照。与单独的食物+ E-IH相比，联合HFD和E-IH治疗没有进一步损害血管舒张。血管舒张反应正常化的抗氧化剂EUK-134在每个treatment group.ConclusionsIncreased肥胖和模拟睡眠呼吸暂停损害内皮依赖性血管舒张，通过增强生成的活性氧（ROS）。然而，联合治疗不会加剧ROS生成或单独使用HFD或E-IH观察到的血管功能障碍。
BackgroundAlthough there often is a clinical co-incidence of increased adiposity and obstructive sleep apnea, each factor is independently associated with elevated oxidative stress.ObjectiveWe hypothesized that overweight rats exposed to simulated sleep apnea would develop exacerbated oxidative stress leading to impaired endothelium-dependent vasodilation.MethodsRats were fed either a chow or high-fat diet (HFD; 60% kcal from fat) for 6 weeks. During the final 14 days of each diet, animals were exposed to either air or eucapnic intermittent hypoxia (E-IH) to simulate sleep apnea.ResultsRats exposed to either E-IH or HFD alone showed increases of 161 and 176%, respectively, in oxidative stress (measured as thiobarbituric acid-reactive substances) compared to chow+ air controls. However, oxidative stress was lower following combined HFD+ E-IH treatment (132% of chow+ air controls) compared to each individual treatment. All three treatment groups, chow+ E-IH, HFD+ air and HFD+ E-IH, had increased blood pressure (144.5±4.4, 148.2±5.6, and 136.2±2.0 mm Hg, respectively, vs. chow+ air: 123±2.0 mm Hg) and attenuated acetylcholine (ACh)-mediated vasodilation (78.3, 72.7, and 78.2% of the chow+ air response at the highest dose of ACh) compared to chow+ air controls. Combined HFD and E-IH treatment did not further impair vasodilation compared to chow+ E-IH alone. Vasodilatory responses were normalized by the antioxidant EUK-134 in each treatment group.ConclusionsIncreased adiposity and simulated sleep apnea impair endothelium-dependent vasodilation through enhanced generation of reactive oxygen species (ROS). However, the combined treatment does not exacerbate either ROS generation or vascular dysfunction observed with HFD or E-IH alone.