Plasma volume restoration with salt tablets and water after bed rest prevents orthostatic hypotension and changes in supine hemodynamic and endocrine variables.
Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.
Waters
Wendy W
WW
Human Adaptation and Countermeasures Office, Wyle Laboratories, Inc., Houston, Texas, USA.
Platts
Steven H
SH
Mitchell
Brett M
BM
Whitson
Peggy A
PA
Meck
Janice V
JV
D000328:Adult; D000450:Aldosterone / Q000097:blood; D017704:Baroreflex / Q000502:physiology; D001510:Bed Rest / Q000009:adverse effects*; D001794:Blood Pressure / Q000502:physiology; D004326:Drinking; D004703:Endocrine System / Q000502:physiology; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010953:Plasma Volume / Q000502:physiology*; D011941:Receptors, Adrenergic / Q000502:physiology; D012083:Renin / Q000097:blood; D012965:Sodium Chloride / Q000008:administration & dosage*; D013026:Space Flight; D013318:Stroke Volume / Q000502:physiology; D016683:Supine Position; D014655:Vascular Resistance / Q000502:physiology; D014667:Vasopressins / Q000097:blood; D018474:Weightlessness Simulation / Q000009:adverse effects
D011941:Receptors, Adrenergic; D014667:Vasopressins; D012965:Sodium Chloride; D000450:Aldosterone; D012083:Renin; D009638:Norepinephrine; D004837:Epinephrine