PLASMA HYPEROSMOLALITY AND ARTERIAL-PRESSURE REGULATION DURING HEATING IN DEHYDRATED AND AWAKE RATS

Citation
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
Citations number
47
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
44
Issue
5
Year of publication
1998
Pages
1703 - 1711
Database
ISI
SICI code
0363-6119(1998)44:5<1703:PHAARD>2.0.ZU;2-P
Abstract
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.