Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas.
J Appl Physiol (1985). 2021 Mar 1;130(3):846-852. doi: 10.1152/japplphysiol.00772.2020. Epub 2021 Jan 7.
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. The aim of the present study was to determine whether an acute bout of intermittent hypoxia protects against an ischemia-reperfusion injury in young healthy individuals. Brachial artery endothelial function was assessed by flow-mediated dilation in 16 young healthy individuals before and after a 20-min upper arm 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-min hypoxic cycles at an arterial oxygen saturation of 87 ± 3% separated by 4-min normoxic cycles. Intermittent hypoxia resulted in a lower arterial oxygen saturation than intermittent normoxia (hypoxia: 87 ± 3% vs. normoxia: 99 ± 1%, < 0.01), which was equivalent to a lower fraction of inspired oxygen (hypoxia: 0.123 ± 0.013 and normoxia: 0.210 ± 0.003, < 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% and normoxia: 7.1 ± 2.5 to 4.0 ± 2.4%, time × condition interaction = 0.048). Exposure to intermittent hypoxia did not affect mean arterial pressure (hypoxia: 92 ± 9 mmHg and normoxia: 89 ± 8 mmHg, = 0.19) or cardiac output (hypoxia: 5.8 ± 1.1 L·min and normoxia: 5.3 ± 1.1 L·min, = 0.29). In conclusion, 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. Ischemia-reperfusion injury induced by restoration of blood flow following occlusion impairs flow-mediated dilation, a marker of endothelium-dependent vasodilation. In young healthy adults, exposure to intermittent hypoxia, consisting of alternating short bouts of breathing hypoxic and normoxic air, before an ischemia-reperfusion injury significantly attenuated the reduction in flow-mediated dilation. Thus, hypoxic preconditioning represents a potential strategy to mitigate the effect of ischemia-reperfusion injury associated with ischemic events.
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。短暂的全身低氧血症同样可以减轻缺血再灌注损伤引起的血管舒张反应迟钝。本研究的目的是确定急性间歇性缺氧是否能保护年轻健康个体免受缺血再灌注损伤。在 16 名年轻健康个体的肱动脉血流阻塞 20 分钟以诱导缺血再灌注损伤之前和之后，通过血流介导的扩张来评估肱动脉内皮功能。血流阻塞之前进行间歇性低氧或间歇性常氧处理。间歇性低氧由三个动脉血氧饱和度为 87±3%的低氧周期组成，每个低氧周期之间夹有 4 分钟的常氧周期。间歇性低氧导致的动脉血氧饱和度低于间歇性常氧（低氧：87±3% vs. 常氧：99±1%， < 0.01），这相当于吸入氧分数较低（低氧：0.123±0.013 vs. 常氧：0.210±0.003， < 0.01）。在间歇性常氧预处理之前，血流阻塞导致血流介导的扩张减弱。相比之下，先前暴露于间歇性低氧可减轻血流阻塞后血流介导的扩张减少（低氧：6.4±1.9%至 4.4±2.3%和常氧：7.1±2.5%至 4.0±2.4%，时间×条件交互作用=0.048）。间歇性低氧暴露不会影响平均动脉压（低氧：92±9mmHg 和常氧：89±8mmHg，=0.19）或心输出量（低氧：5.8±1.1L·min 和常氧：5.3±1.1L·min，=0.29）。总之，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减少。间歇性低氧代表了一种减轻与缺血事件相关的缺血再灌注损伤影响的潜在策略。阻塞后血流恢复引起的缺血再灌注损伤会损害血流介导的扩张，这是一种内皮依赖性血管舒张的标志物。在年轻健康成年人中，在缺血再灌注损伤之前，进行间歇性低氧处理（由短暂的短时间呼吸低氧和常氧空气交替组成）可显著减轻血流介导的扩张减少。因此，低氧预处理代表了一种减轻与缺血事件相关的缺血再灌注损伤影响的潜在策略。
