Glaister D H, Miller N L
Crew Technology Division, USAF School of Aerospace Medicine, Brooks AFB, TX.
Aviat Space Environ Med. 1990 Feb;61(2):99-105.
Cerebral oxygen sufficiency was studied noninvasively, using multiwavelength near-infrared spectrophotometry, in eight subjects exposed to lower body negative pressure (LBNP) of up to -90 mm Hg to induce presyncopal symptoms and signs. LBNP caused only small changes in the forebrain measures until the last 60 s of the exposures, whereupon oxyhemoglobin (HbO2) and oxidised cytochrome c oxidase fell, reduced hemoglobin (Hb) rose slightly, and the tissue blood volume (HbO2 + Hb) fell. In subjects showing presyncope, these changes anticipated the onset of a terminal bradycardia by some 20 s and may provide the trigger for cardiovascular decompensation, while the cessation of LBNP led to an overshoot in cerebral blood volume suggestive of a reactive hyperemia. Psychomotor testing showed a significant slowing of reaction time with LBNP, but only for the easiest component of a complex task, while saccadic latencies were found to be shortened following LBNP exposure.
采用多波长近红外分光光度法，对8名受试者进行了无创性脑氧充足性研究。这些受试者暴露于高达-90 mmHg的下体负压（LBNP）下，以诱发晕厥前期症状和体征。在暴露的最后60秒之前，LBNP仅引起前脑测量值的微小变化，随后氧合血红蛋白（HbO2）和氧化型细胞色素c氧化酶下降，还原血红蛋白（Hb）略有上升，组织血容量（HbO2 + Hb）下降。在出现晕厥前期的受试者中，这些变化比终末期心动过缓的发作提前约20秒，可能是心血管失代偿的触发因素，而停止LBNP会导致脑血容量过冲，提示反应性充血。心理运动测试显示，LBNP会使反应时间显著减慢，但仅针对复杂任务中最简单的部分，而扫视潜伏期在LBNP暴露后缩短。
