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1 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan; Department of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Aichi, Japan
2 Department of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Aichi, Japan
3 Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Science, Nagoya, Aichi, Japan
4 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan
* To whom correspondence should be addressed. E-mail: kamiya{at}ri.ncvc.go.jp.
Although orthostatic hypotension is a common clinical syndrome after spaceflight, the pathophysiology remains unclear both for it and its ground-based simulation model, 6° head-down bed rest (HDBR). The authors' hypothesis, that a decrease in sympathetic nerve activity is the major pathophysiology underlying orthostatic hypotension following HDBR, was tested in a study involving 14-day HDBR in 22 healthy subjects who showed no orthostatic hypotension during 15-minutes 60° head-up tilt test (HUT) at baseline. After HDBR, 10 of 22 subjects demonstrated orthostatic hypotension during 60° HUT. In subjects with orthostatic hypotension, total activity of muscle sympathetic nerve activity (MSNA) increased less during the first minute of 60° HUT after HDBR (314% of resting supine activity) than before HDBR (523% of resting supine activity, P<0.05), despite HDBR-induced reduction in plasma volume (13% of plasma volume before HDBR). The postural increase in total MSNA continued during a further several minutes of 60° HUT while arterial pressure was maintained. Thereafter, however, total MSNA was paradoxically suppressed by 104% of the resting supine level at the last minute of HUT (P<0.05 vs. earlier 60° HUT periods). The suppression of total MSNA was accompanied by a 22 ± 4 mm Hg decrease in mean blood pressure (systolic blood pressure <80 mmHg). In contrast, orthostatic activation of total MSNA was preserved throughout 60° HUT in subjects who did not develop orthostatic hypotension. The data gathered support the hypothesis that a decrease in sympathetic nerve activity is the major pathophysiology underlying orthostatic hypotension after HDBR. It appears that the diminished sympathetic activity, in combination with other factors associated with HDBR (e.g., hypovolemia) may predispose some individuals to postural hypotension.
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