Y. Nakajima et al., PLASMA HYPEROSMOLALITY AND ARTERIAL-PRESSURE REGULATION DURING HEATING IN DEHYDRATED AND AWAKE RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 44(5), 1998, pp. 1703-1711
To gain better insights into the effect of dehydration on thermal and
cardiovascular regulation during hyperthermia, we examined these regul
atory responses during body heating in rats under isosmotic hypovolemi
a and hyperosmotic hypovolemia. Rats were divided into four groups: no
rmovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma vol
ume loss (Delta PV) = -20% of control], hypovolemic and less hyperosmo
tic [HL1, increase in plasma osmolality (Delta P-osm) = 23 mosmol/kgH(
2)O, Delta PV = -16%], and hypovolemic and more hyperosmotic (HL2, Del
ta P-osm = 52 mosmol/kgH(2)O, Delta PV = -17%). Hyperosmolality was at
tained by subcutaneous injection of hypertonic saline and hypovolemia
by intra-arterial injection of furosemide before heating, Then rats we
re placed in a thermocontrolled box (35 degrees C air temperature, sim
ilar to 20% relative humidity) for 1-2 h until rectal temperatures (T-
re) reached 40.0 degrees C. Mean arterial pressure in L decreased with
rise in T-re (P < 0.001), whereas mean arterial pressure remained con
stant in the other groups. Maximal tail skin blood flow in L, HL1, and
HL2 was decreased to similar to 30% of that in C (P < 0.001). T-re th
reshold for tail skin vasodilation (TVD) was not changed in L, whereas
the threshold shifted higher in the HL groups. T-re threshold for TVD
was highly correlated with P-osm (r = 0.94, P < 0.001). Heart rate in
the HL groups increased with rise in T-re (P < 0.001), whereas it rem
ained unchanged in C and L. Cardiovascular responses to heating were n
ot influenced by V-1 antagonist in C, L, and HL2. Thus isotonic hypovo
lemia attenuates maximal tail skin blood flow, whereas hypertonic hypo
volemia causes an upward shift of T-re threshold for TVD and an increa
se in heart rate during hyperthermia. These results suggest that plasm
a hyperosmolality stimulates presser responses in the hypovolemic cond
ition that subsequently contribute to arterial pressure regulation dur
ing heat stress.