引起应激反应的高+Gz加速度有关。然而,在如此条件下加速度引起意识丧失(G-LOC)的机理尚未确立。我们假定大脑缺血与缺氧以及有联系的神经生理学的机能障碍可能是引起G-LOC的重要因素。方法 我们用吸氧的新西兰白兔进行实验。脑的氧合用近红外分光镜(NIRS)进行连续的无创性监测,并一起监测心电图、中心动脉血压、脑电图(EEG)与脑干听觉诱发电位(BAEP)。通过首先使双侧颈动脉闭塞,接着附加闭塞椎动脉与颈静脉(CVJO)以致缺血。通过改变O_2与N_2O混合气引起渐进性的缺氧,直到O_2浓度为零产生 The stress-induced high + Gz acceleration. However, the mechanism of acceleration-induced loss of consciousness (G-LOC) under such conditions has not been established. We hypothesized that ischemia and hypoxia in the brain and associated neurophysiologic dysfunction may be important factors in G-LOC. Methods We performed experiments with oxygen-absorbing New Zealand white rabbits. Oxygenation of the brain Continuous noninvasive monitoring with near infrared spectroscopy (NIRS) and monitoring of electrocardiogram, central arterial pressure, electroencephalogram (EEG) and brainstem auditory evoked potential (BAEP). Ischemia was achieved by first occluding both carotid arteries followed by occlusion of the vertebral artery and jugular vein (CVJO). Progressive hypoxia is induced by changing O 2 and N 2 O mixtures until O 2 concentration is zero