F. Baisch et al., Cardiovascular response to lower body negative pressure stimulation before, during, and after space flight, EUR J CL IN, 30(12), 2000, pp. 1055-1065
Citations number
22
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Background It is well known that space travel cause post-flight orthostatic
hypotension and it was assumed that autonomic cardiovascular control deter
iorates in space. Lower body negative pressure (LBNP) was used to asses aut
onomic function of the cardiovascular system.
Methods LBNP tests were performed on six crew-members before and on the fir
st days post-flight in a series of three space missions. Additionally, two
of the subjects performed LBNP tests in-flight. LBNP mimics fluid distribut
ion of upright posture in a gravity independent way. It causes an artificia
l sequestration of blood, reduces preload, and filtrates plasma into the lo
wer part of the body. Fluid distribution was assessed by bioelectrical impe
dance and anthropometric measurements.
Results Heart rate, blood pressure, and total peripheral resistance increas
ed significantly during LBNP experiments in-flight. The decrease in stroke
volume, the increased pooling of blood, and the increased filtration of pla
sma into the lower limbs during LBNP indicated that a plasma volume reducti
on and a deficit of the interstitial volume of lower limbs rather than a ch
ange in cardiovascular control was responsible for the in-flight response.
Post-flight LBNP showed no signs of cardiovascular deterioration. The still
more pronounced haemodynamic changes during LBNP reflected the expected be
haviour of cardiovascular control faced with less intravascular volume. In-
flight, the status of an intra-and extravascular fluid deficit increases sy
mpathetic activity, the release of vasoactive substances and consequently b
lood pressure. Post-flight, blood pressure decreases significantly below pr
e-flight values after restoration of volume deficits.
Conclusion We conclude that the cardiovascular changes in-flight are a cons
equence of a fluid deficit rather than a consequence of changes in autonomi
c signal processing.