Cardiac output distribution in thermally dehydrated rodents.

The effect of thermal dehydration (37 degrees C) on the integrated response of the circulation was studied in conscious laboratory rats and in the desert species Psammomys obesus, the latter being studied prior to and following acclimation to heat. Cardiac output (CO) and its distribution were measured using labeled microspheres with the reference organ technique. At low dehydration (7-9% body wt loss) rats showed peripheral vasodilation coincidentally with splanchnic vasoconstriction, whereas the desert species exhibited an increased CO and peripheral vasodilation with no change in splanchnic blood perfusion. At severe dehydration (10-18% body wt loss), closure of skin arteriovenous anastomoses together with splanchnic vasodilation was observed in both species. These changes were discussed in relation to plasma volume conservation mechanism and its deterioration. Acclimation to heat resulted in no change in CO, whereas blood flow to splanchnic and skin capillaries increased remarkably. Dehydration in heat-acclimated P. obesus (5-10% body wt loss) brought about a significant fall in CO. However, most organs maintained relatively stable blood flow. This might contribute to better survival during heat stress.