STUDY OBJECTIVES Obstructive sleep apnea (OSA) is a sleep disorder caused by transient obstruction of the upper airway and results in intermittent hypoxia, sleep fragmentation, sympathetic nervous system activation, and arousal which can have an adverse effect on cardiovascular disease. It is theorized that OSA might intensify stroke injury. Our goal here was to develop a new model of experimental OSA and test its ability to aggravate behavioral and morphological outcomes following transient brain ischemia/reperfusion. METHODS We used a 3D printed OSA device to expose C57BL6 mice to 3 h of OSA (obstructive apnea index of 20 events per hour) for three days. These mice were then subjected to ischemia/reperfusion using the middle cerebral artery occlusion model (MCAO) stroke and examined for overall survival, infarct size and neurological scoring. RESULTS We found that OSA transiently decreased respiration and reduced oxygen saturation with bradycardia and tachycardia typical of human responses during apneic events. Brain injury from MCAO was significantly increased by OSA as measured by infarct size and location as well as by intensification of neurological deficits; mortality following MCAO was also increased in OSA animals. CONCLUSIONS Our findings suggest that our new model of OSA alters respiratory and cardiovascular physiological functions and is associated with enhanced ischemia/reperfusion mediated injury in our non-invasive, OSA intensified model of stroke.

中文翻译：

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阻塞性睡眠呼吸暂停会加重大脑中动脉闭塞后的中风严重程度。

研究目的阻塞性睡眠呼吸暂停（OSA）是由上呼吸道短暂阻塞引起的睡眠障碍，导致间歇性缺氧，睡眠破碎，交感神经系统激活和唤醒，可能对心血管疾病产生不利影响。从理论上讲，OSA可能加剧中风损伤。我们的目标是建立实验性OSA的新模型，并测试其在短暂性脑缺血/再灌注后加重行为和形态结果的能力。方法我们使用3D打印OSA设备将C57BL6小鼠暴露于3小时的OSA（每小时20个事件的阻塞性呼吸暂停指数）中，持续三天。然后，使用大脑中动脉闭塞模型（MCAO）对这些小鼠进行缺血/再灌注，并检查其总体存活率，梗塞面积和神经学评分。结果我们发现OSA会暂时性地减少呼吸，并降低呼吸暂停事件中典型的人类心动过缓和心动过速引起的氧饱和度。OSA显着增加了MCAO引起的脑损伤，这通过梗死面积和位置以及神经功能缺损的加剧来衡量。OSA动物中MCAO后的死亡率也增加。结论我们的发现表明，在我们的非侵入性，OSA强化中风模型中，我们的OSA新模型改变了呼吸和心血管的生理功能，并与缺血/再灌注介导的损伤增强有关。OSA显着增加了MCAO引起的脑损伤，这通过梗死面积和位置以及神经功能缺损的加剧来衡量。OSA动物中MCAO后的死亡率也增加。结论我们的发现表明，在我们的非侵入性，OSA强化中风模型中，我们的OSA新模型改变了呼吸和心血管的生理功能，并与缺血/再灌注介导的损伤增强有关。OSA显着增加了MCAO引起的脑损伤，这通过梗死面积和位置以及神经功能缺损的加剧来衡量。OSA动物中MCAO后的死亡率也增加。结论我们的发现表明，在我们的非侵入性，OSA强化中风模型中，我们的OSA新模型改变了呼吸和心血管的生理功能，并与缺血/再灌注介导的损伤增强有关。