Aims: 

Under conditions of heat stress and hyperosmotic dehydration, both animals and humans reduce thermoregulatory evaporation and regulate deep body temperature at elevated levels. Hyperosmotic dehydration attenuates the heat stress-induced cutaneous vasodilatation. However, little is known about the effects of hypovolemia/isosmotic dehydration on cardiorespiratory responses to hyperthermia.

Methods: 

Therefore, cardiorespiratory responses to hyperthermia during isosmotic dehydration/hypovolemia were studied in 17 anaesthetized adult rabbits divided into two groups: normovolemic group (NV; n = 10) and hypovolemic group (HV; n = 7). In the HV group, hypovolemia (16% decrease in plasma volume) was induced by furosemide administration (5 mg/kg i. v.).

Results: 

During hyperthermia (the rise in body temperature /BT/ to 42°C by a gradual body surface heating), the HV rabbits had the breathing frequency lower (P < 0.05) than the NV animals. The panting was absent in the HV rabbits at the BT of 42°C, unlike the NV animals. From cardiovascular variables, the vasoconstrictor response in visceral (mesenteric) region during hyperthermia was attenuated (P < 0.05), whereas the heat stress-induced cutaneous vasodilatation was not significantly influenced by hypovolemia.

Conclusion: 

The lower frequency of breathing, thus lower respiratory evaporative heat loss during exogenous hyperthermia in dehydrated animals are present not only during hyperosmotic dehydration, but they occur also under conditions of furosemide-induced isosmotic dehydration/hypovolemia.