I. Assenmacher et al., CHRONIC ORTHOSTATIC AND ANTIORTHOSTATIC RESTRAINT INDUCE NEUROENDOCRINE, IMMUNE AND NEUROPHYSIOLOGICAL DISORDERS IN RATS, Acta astronautica, 36(8-12), 1995, pp. 545-558
The tail-cast suspension rat model has been developed in ground labora
tories interested in space physiology for extensive study of mechanism
s causing the pathophysiological syndrome associated with space flight
s, We used individually-caged male rats to explore the effects of acut
e and chronic (7d) orthostatic restraint (OR) and head-down anti-ortho
static restraint (AOR) on a series of physiological variables; The acu
te restraint study showed that (1) the installation of the OR device i
nduced an acute reaction for 2 days, with a substantial rise in ACTH (
x2) and CORT (x6), and that (2) the head-down tilt from OR to AOR indu
ced (i) within 10 min and lasting 60 min a 2-fold rise in the intra-ce
rebro-ventricular pressure (Picv) monitored with an icy telemetric rec
ording system, which receded to normal between 60 and 120 min; and (ii
) within 30 min a short-lived 4-fold rise in plasma ACTH and CORT leve
ls, Chronic OR induced (1) the suppression of the diurnal ACTH/CORT rh
ythm, with increased mean levels, especially for ACTH, (2) a degraded
circadian locomotor activity rhythm manifested by a significant reduct
ion in the spectral power of the 24h periodicity and a concomitant eme
rgence of shorter (ultradian) periodicities, (3) an associated, but le
ss pronounced alteration of the diurnal rhythm in body temperature; an
d (4) a marked increase in baseline plasma levels of IL-1 beta and an
increased reactivity in cytokine release following an E, coli endotoxi
n (LPS) challenge. AOR induced (1) a similar obliteration of the circa
dian ACTH/CORT rhythm, (2) the loss of close correlation between ACTH
and CORT, (3) a generalized increase in baseline plasma IL-1 beta leve
ls and (4) more extensive degradation of the circadian periodicity for
both locomotor activity and, to a lesser extent, body temperature, re
placed by dominant spectral powers for ultradian periodicities (3 to 1
0 h). In conclusion, both experimental paradigms - but AOR more than O
R - caused a blockade of the circadian rhythmicity of major physiologi
cal variables, the loss of normal correlations between ACTH and CORT,
and inflammatory-immune hyperreactivity. These pathophysiological diso
rders may all be parts of a complex chronic stress syndrome.