Ischemic preconditioning attenuates the reduction in brachial artery endothelial function following an ischemia-reperfusion injury. Brief bouts of systemic hypoxemia could similarly mitigate the blunted vasodilatory response induced by an ischemia-reperfusion injury. AIM: To determine whether an acute bout of intermittent hypoxia protects against an ischemia-reperfusion injury in young healthy individuals. METHODS: Brachial artery endothelial function was assessed by flow-mediated dilation in 16 young healthy individuals before and after a 20-minute blood flow occlusion to induce ischemia-reperfusion injury. Blood flow occlusion was preceded by either intermittent hypoxia or intermittent normoxia. Intermittent hypoxia consisted of three 4-minute hypoxic cycles at a targeted arterial oxygen saturation of 90% separated by 4-minute normoxic cycles. RESULTS: Intermittent hypoxia resulted in a lower arterial oxygen saturation (Hypoxia: 87±3 vs. Normoxia: 99±1%, p<0.01), which was equivalent to a lower fraction of inspired oxygen (Hypoxia: 0.123±0.013, Normoxia: 0.210±0.003, p<0.01). When preceded by intermittent normoxia, blood flow occlusion resulted in a blunted flow-mediated dilation. In contrast, the reduction in flow-mediated dilation following blood flow occlusion was attenuated by prior exposure to intermittent hypoxia (Hypoxia: 6.4±1.9 to 4.4±2.3, Normoxia: 7.1±2.5 to 4.0±2.4%, time x condition interaction p=0.048). Exposure to intermittent hypoxia did not affect mean arterial pressure (Hypoxia: 92±9, Normoxia: 89±8 mmHg, p=0.19) or cardiac output (Hypoxia: 5.8±1.1, Normoxia: 5.3±1.1 L·min^-1, p=0.29). CONCLUSIONS: Hypoxic preconditioning attenuates the reduction in flow-mediated dilation induced by blood flow occlusion in young healthy individuals. Intermittent hypoxia represents a potential strategy to mitigate the effect of ischemia-reperfusion injury associated with ischemic events.

中文翻译：

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缺氧预处理可减轻年轻健康成年人的缺血再灌注损伤

缺血预处理可减轻缺血再灌注损伤后肱动脉内皮功能的降低。短暂的全身性低氧血症发作可以类似地减轻由缺血-再灌注损伤引起的钝化血管舒张反应。目的：确定急性间歇性缺氧是否可以预防年轻健康个体的缺血再灌注损伤。方法：通过血流介导的扩张，在20分钟血流阻塞诱发缺血再灌注损伤之前和之后，通过流动介导的扩张来评估肱动脉内皮功能。间歇性缺氧或间歇性常氧之前是血流阻塞。间歇性缺氧由三个4分钟的缺氧循环组成，目标动脉氧饱和度为90％，间隔4分钟为正常氧循环。结果：间歇性低氧导致较低的动脉血氧饱和度（低氧：87±3 vs.正常氧：99±1％，p <0.01），相当于较低的吸入氧分数（低氧：0.123±0.013，正常氧： 0.210±0.003，p <0.01）。在间歇性常氧之前，血流阻塞导致钝化的血流介导的扩张。相比之下，血流阻塞后血流介导的扩张减少因先前暴露于间歇性缺氧而减弱（低氧：6.4±1.9至4.4±2.3，常氧：7.1±2.5至4.0±2.4％，时间x条件相互作用p = 0.048）。间歇性缺氧不会影响平均动脉压（低氧：92±9，常氧：89±8 mmHg，p = 0.19）或心输出量（低氧：5.8±1.1，常氧：5.3±1.1 L·min 相对于正常氧为87±3：99±1％，p <0.01），相当于较低比例的吸入氧气（低氧：0.123±0.013，正常氧：0.210±0.003，p <0.01）。在间歇性常氧之前，血流阻塞导致钝化的血流介导的扩张。相比之下，血流阻塞后血流介导的扩张减少因先前暴露于间歇性缺氧而减弱（低氧：6.4±1.9至4.4±2.3，常氧：7.1±2.5至4.0±2.4％，时间x条件相互作用p = 0.048）。间歇性缺氧不会影响平均动脉压（低氧：92±9，常氧：89±8 mmHg，p = 0.19）或心输出量（低氧：5.8±1.1，常氧：5.3±1.1 L·min 相对于正常氧为87±3：99±1％，p <0.01），相当于较低比例的吸入氧气（低氧：0.123±0.013，正常氧：0.210±0.003，p <0.01）。在间歇性常氧之前，血流阻塞导致钝化的血流介导的扩张。相比之下，血流阻塞后血流介导的扩张减少因先前暴露于间歇性缺氧而减弱（低氧：6.4±1.9至4.4±2.3，常氧：7.1±2.5至4.0±2.4％，时间x条件相互作用p = 0.048）。间歇性缺氧不会影响平均动脉压（低氧：92±9，常氧：89±8 mmHg，p = 0.19）或心输出量（低氧：5.8±1.1，常氧：5.3±1.1 L·min 在间歇性常氧之前，血流阻塞导致钝化的血流介导的扩张。相比之下，血流阻塞后血流介导的扩张减少因先前暴露于间歇性缺氧而减弱（低氧：6.4±1.9至4.4±2.3，常氧：7.1±2.5至4.0±2.4％，时间x条件相互作用p = 0.048）。间歇性缺氧不会影响平均动脉压（低氧：92±9，常氧：89±8 mmHg，p = 0.19）或心输出量（低氧：5.8±1.1，常氧：5.3±1.1 L·min 在间歇性常氧之前，血流阻塞导致钝化的血流介导的扩张。相比之下，血流阻塞后血流介导的扩张减少因先前暴露于间歇性缺氧而减弱（低氧：6.4±1.9至4.4±2.3，常氧：7.1±2.5至4.0±2.4％，时间x条件相互作用p = 0.048）。间歇性缺氧不会影响平均动脉压（低氧：92±9，常氧：89±8 mmHg，p = 0.19）或心输出量（低氧：5.8±1.1，常氧：5.3±1.1 L·min^-1，p ＝ 0.29）。结论：低氧预处理可减轻年轻健康个体血流阻塞引起的血流介导的扩张的减少。间歇性缺氧代表减轻与缺血事件相关的缺血再灌注损伤的潜在策略。