Cerebral tissue oxygen status and psychomotor performance during lower body negative pressure ( LBNP).
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.[1]References
- Cerebral tissue oxygen status and psychomotor performance during lower body negative pressure (LBNP). Glaister, D.H., Miller, N.L. Aviation, space, and environmental medicine. (1990) [Pubmed]
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