F-12J Free Communication/Thematic Poster Space Flight and Bed Rest Deconditioning
With the removal of gravitational hydrostatic gradients during spaceflight or bed rest, there is a shift of intravascular fluid from the lower body to the head, which leads to altered cerebral autoregulation in animals and humans. We hypothesized that these changes in cerebral pressure-flow regulation would be accompanied by similar changes in metabolic cerebral vasomotor reactivity. To test this hypothesis, we measured the responses of cerebral blood flow (CBF) velocity (transcranial Doppler) to hypercapnic stimuli of 3 and 6% CO2 breathing in 13 healthy subjects before and after 2-weeks of head-down tilt (HDT) bed rest. Arterial pressure was monitored by photoplethysmography (Finapres). End-tidal CO2 (PETCO2) was monitored by infrared capnograph. Cerebral vasomotor reactivity was quantified by the slope of linear regression of percent changes in CBF velocity vs. PETCO2 (mmHg). Cerebrovascular resistance index (CVRI) was calculated as mean arterial pressure divided by mean CBF velocity.
in response to 3 and 6% CO2, CBF velocity increased significantly by 11 ± 3 and 54 ±3% before, and by 20 ± 5 and 72 ± 3% after bed rest (P <0.05). Simultaneously, CVRI decreased significantly both before and after bed rest in response to CO2 (P <0.05). However, cerebral vasomotor reactivity before and after bed rest remained unchanged (before: 3.89 ± 0.26; after: 3.57 ± 0.31 CBF%/mmHg). These findings indicate that cerebrovascular responses to hypercapnic stimuli are not altered by short-term HDT bed rest. We suspect that the functional integrity of cerebral vasomotor reactivity is preserved after adaptation of the cerebral circulation to real and/or simulated microgravity in humans.