Effect of human head flexion on the control of peripheral blood flow in microgravity and in 1 g.

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.