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首页> 外文期刊>American Journal of Physiology >UBC-Nepal Expedition: imposed oscillatory shear stress does not further attenuate flow-mediated dilation during acute and sustained hypoxia
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UBC-Nepal Expedition: imposed oscillatory shear stress does not further attenuate flow-mediated dilation during acute and sustained hypoxia

机译：UBC-尼泊尔探险：施加的振荡剪切应力在急性和持续的缺氧期间不再衰减流动介导的扩张

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Experimentally induced oscillatory shear stress (OSS) and hypoxia reduce endothelial function in humans. Acute and sustained hypoxia may cause increases in resting OSS; however, whether this influences endothelial susceptibility to further increases in OSS is unknown. Healthy lowlanders (n = 15, 30?±?6 yr; means?±?SD) participated in three OSS interventions: two interventions at sea level [normoxia and after 20 min of normobaric hypoxia (acute hypoxia, 11% O2)] and one intervention 5–7 days after a 9-day ascent to 5,050 m (sustained hypoxia). OSS was provoked in the brachial artery using a 30-min distal cuff inflation (75 mmHg). Endothelial function was assessed before and after each intervention by reactive hyperemia flow-mediated dilation (FMD). Shear stress magnitude and patterns were obtained via Duplex ultrasound. Baseline retrograde shear stress and OSS were greater in acute hypoxia versus normoxia (P < 0.001), and OSS was elevated in sustained hypoxia versus normoxia (P = 0.011). The intervention further augmented OSS during each condition. Preintervention FMD was decreased by 29?±?48% in acute hypoxia and by 25?±?31% in sustained hypoxia compared with normoxia (P = 0.001 and 0.026); these changes correlated with changes in baseline mean and antegrade shear stress. After the intervention, FMD decreased during normoxia (?41?±?26%, P < 0.001) and was unaltered during acute or sustained hypoxia. Therefore, a 30-min exposure to OSS reduced FMD during normoxia, a condition with an unchallenged, healthy endothelium; however, imposed OSS did not appear to worsen endothelial function during acute or sustained hypoxia. Exposure to an altered magnitude and pattern of shear stress at baseline in hypoxia may contribute to the insensitivity to further acute augmentation of OSS.NEW & NOTEWORTHY We investigated whether the endothelium remains sensitive to experimental increases in oscillatory shear stress in acute (11% O2) and sustained (2 wk at 5,050 m) hypoxia. Hypoxia altered baseline shear stress and decreased endothelial function (flow-mediated dilation); however, exposure to experimentally induced oscillatory shear stress only impaired flow-mediated dilation in normoxia.
机译：实验诱导振荡剪切应力（OSS）和缺氧降低人类内皮功能。急性和持续的缺氧可能导致休息的OSS增加;但是，这是否会影响进一步增加OSS的内皮易感性未知。健康的低地人（n = 15,30？±6年;手段？一个干预5-7天后9天的上升至5,050米（持续缺氧）。使用30分钟的远端袖带通胀（75 mmHg）在肱动脉中引发OSS。在每次干预之前和之后评估内皮功能，通过反应性高血量介导的扩张（FMD）。通过双相超声获得剪切应力幅度和图案。基线逆行剪切应力和OSS在急性缺氧与常氧（P <0.001）中更大，并且OSS在持续的缺氧与常氧（P = 0.011）中升高。在每个条件下，干预进一步增强了OSS。急性缺氧中急性缺氧的预领素±48％降低，与常氧相比，持续缺氧的25℃（p = 0.001和0.026）;这些变化与基线平均值和方剪应力的变化相关。干预后，FMD在常氧（α41？±26％，P <0.001）期间减少，并且在急性或持续的缺氧期间未妨碍。因此，在常氧期间，30分钟暴露于OSS减少FMD，一种含有未经充电的健康内皮的病症;然而，施加的OSS在急性或持续的缺氧期间没有似乎恶化内皮功能。暴露于缺氧基线的改变的幅度和剪切应力模式可能有助于进一步急性增强O之间的不敏感性.New和值得注意的是我们研究了内皮是否对急性振荡剪切应力的实验性增加敏感（11％O2）并持续（2周为5,050米）缺氧。缺氧改变基线剪切应力并降低内皮功能（流动介导的扩张）;然而，暴露于实验诱导的振荡剪切应力仅在常氧中的流动介导的扩张仅受损。

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