Abstract
This study evaluated, in six healthy subjects, whether head flexion, which stimulates the vestibular system and the tonic neck receptors, interferes with cardiovascular regulation. Arterial parameters were measured continuously using a pulsed Doppler ultrasound probe during parabolic flights with subjects either in the supine craned-head position (control) or in the supine anterior neck flexion bent-neck position. Exposure to 0 g induced a fluid shift towards the head (stroke volume +8%, P<0.05). Compared to the control situation the mean (SD) blood flow in the femoral artery decreased [ -10 (9)% vs +1 (10)%; P<0.05], and the ratio cerebral artery:femoral artery blood flow ( : ) increased [+8 (14)% vs -4 (7)%; P<0.05], in the bent-neck position. Thus, neck flexion without otolith loading (subject in 0 g) favoured cerebral perfusion during the exposure to 0 g. The return to 1 g, even in the supine position, induced a fluid shift towards the lower limbs. From 0 to 1 g, reduced less [ +6 (8)% vs -1 (8)%; P<0.05], and the : decreased more [-11 (9)% vs 0 (10)%; P<0.05], in the bent-neck position than in the control position. Thus the redistribution of peripheral blood flow in response to the fluid shift towards the legs was less efficient in the bent-neck position. In 0 g environment the passive flexion of the neck (neck receptor stimulation only) increased resistance in the femoral artery [ R(fa) +20 (21)%; P<0.05] and reduced the [-15(10)%; P<0.07] which increased the redistribution of flow towards the brain [; +12 (7)%; P<0.07]. This response was of lower amplitude when both otoliths and neck muscle were stimulated (neck flexion in 1 g) [ R(fa)+9 (7)%, P<0.05; -9 (12), NS; : 0 (12), NS]. We suggest that otolith and neck muscle stimulation (by neck flexion) trigger opposite vascular effects in response to a fluid shift towards the legs.
Published Version
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