To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (ΔPV) = −20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (ΔPosm) = 23 mosmol/kgH2O, ΔPV = −16%], and hypovolemic and more hyperosmotic (HL2, ΔPosm = 52 mosmol/kgH2O, ΔPV = −17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35°C air temperature, ∼20% relative humidity) for 1–2 h until rectal temperatures (Tre) reached 40.0°C. Mean arterial pressure in L decreased with rise in Tre( P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to ∼30% of that in C ( P < 0.001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Trethreshold for TVD was highly correlated with Posm( r = 0.94, P < 0.001). Heart rate in the HL groups increased with rise in Tre( P < 0.001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.
Model Predictive Control of Drug Infusion System for Mean Arterial Pressure Regulation of Critical Care Patients
