Fever was induced by the intravenous injection of 0.25 microgram/kg of lipopolysaccharide (LPS) from Escherichia coli in eight conscious sheep exposed to ambient temperatures adjusted to the lower range of thermoneutrality. Chronic spinal or hypothalamic thermodes were perfused with water of 44 degrees C for 20 min or for most of the rising phase of fever (100 min of the mean 166 min total rise time). The effects of spinal and hypothalamic heating were identical. Thus, before LPS, spinal or hypothalamic heating did not affect the rate of O2 consumption (VO2) but increased skin blood flow (as indicated by skin temperatures) and elicited panting; therefore rectal temperature (Tre) fell. During fever rise, the already reduced skin blood flow and respiratory rate were not affected by spinal or hypothalamic heating, but the increased VO2 was reduced; consequently, the rise in Tre was attenuated. During the plateau phase of fever, all responses were similar to those seen before LPS. In febrilysis, heating strongly enhanced the operating heat loss mechanisms and, hence, augmented the fall in Tre. Thus, although the thermoeffectors activated by spinal or hypothalamic heating were modified during the different stages of fever, the effect on body temperature was nearly the same. Therefore there seems to be no change in spinal or hypothalamic thermosensitivity during fever in sheep.
Hypothalamic thermosensitivity in capsaicin-desensitized rats.
