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School of Kinesiology, University of Western Ontario, London, Ontario, Canada N6A 3K7
Humans exposed to real or simulated
microgravity experience decrements in blood pressure regulation during
orthostatic stress that may be related to autonomic dysregulation
and/or hypovolemia. We examined the hypothesis that hypovolemia,
without the deconditioning effects of bed rest or spaceflight, would
augment the sympathoneural and vasomotor response to graded orthostatic
stress. Radial artery blood pressure (tonometry), stroke volume (SV),
brachial blood flow (Doppler ultrasound), heart rate
(electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA;
microneurography), and estimated central venous pressure (CVP) were
recorded during five levels (
5,
10,
15,
20 and
40 mmHg)
of randomly assigned lower body negative pressure (LBNP)
(n = 8). Forearm (FVR) and total peripheral vascular
resistance (TPR) were calculated. The test was repeated under randomly
assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an
~16% reduction in plasma volume. Compared with normovolemia, SV and
cardiac output were reduced by ~12% and ~10% at baseline and
during LBNP after the diuretic. During hypovolemia, there was an upward
shift in the %
MSNA/
CVP,
FVR/
CVP, and
TPR/
CVP
relationships during 0 to
20 mmHg LBNP. In contrast to normovolemia,
blood pressure increased at
40 mmHg LBNP during hypovolemia due to
larger gains in the %
MSNA/
CVP and
TPR/
CVP relationships.
It was concluded that acute hypovolemia augmented the neurovascular
component of blood pressure control during moderate orthostasis,
effectively compensating for decrements in SV and cardiac output.
baroreflex; muscle sympathetic nerve activity; Doppler ultrasound; lower body negative pressure; vascular resistance; spironolactone
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