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.