The objective of this test was to measure plasma volume to aid in the proper assessment of hemodynamic parameters, vascular responses, and cardiac size and function. The investigators hypothesized that plasma volume losses will be similar to those following space flight. They expected to see changes in blood volume for subjects following extended periods of bed rest.
APPROACH:
Plasma volume was measured by the carboxyhemoglobin rebreathing method. The test subject breathed into a mouthpiece into which 60 cc of carbon monoxide (CO) was injected. In addition, blood draws were completed before and 10 minutes after CO administration.
RESULTS:
This experiment has concluded. Preliminary results are available.
Interim results were published from Campaign 3 using thirteen subjects which were studied before and during bed rest. Statistical analysis was limited to the first 49-60 days of bed rest and compared to pre-bed rest data. Ultrasound data were collected on vascular and cardiac structure and function. Tilt testing was conducted for 30 minutes or until presyncopal symptoms intervened. Plasma volume was significantly reduced by day seven of bed rest. Flow-mediated dilation in the leg was significantly increased at bed rest day 49. Arterial responses to nitroglycerin differed in the arm and leg, but did not change as a result of bed rest. Anterior tibial artery intimal-medial thickness markedly decreased at bed rest days 21, 35, and 49. Several cardiac functional parameters, including isovolumic relaxation time (73 ms to 85 ms at day 7) and myocardial performance index, were significantly increased during bed rest. There was a trend for decreased orthostatic tolerance following 60 day of bed rest. Over all the data suggest that bed rest altered cardiovascular structure and function in a pattern similar to short-duration spaceflight. Additionally, the vascular alterations were primarily seen in the lower body, while vessels of the upper body were unaffected.
During the artificial gravity (AG) pilot study it was concluded that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.end>