Thermal stimulation of the hypothalamus does not evoke the acute-phase reaction.

Interleukin-1 (IL1) injected into the preoptic-anterior hypothalamus (POAH) induces, besides fever, the hepatic synthesis of acute-phase glycoproteins. Since the febrigenic action of IL1 may involve thermosensitive neurons in the POAH, this study examined whether such neurons also might mediate the acute-phase response (APR). The POAH of six adult NZW rabbits was cooled (Tpo = 34.4 +/- 0.4 degrees C [mean +/- SD]) or heated (40.6 +/- 0.2 degrees C) continuously for 2.5 hr (so as to mimic the mean febrile course following a bolus microinjection of IL1 into the POAH). The ambient temperature (Ta) was 23.5 +/- 1.0 degrees C. Expectedly, core temperature fell and skin temperature rose on POAH heating, and the opposite occurred on POAH cooling. However, no statistically significant changes in the plasma levels of Fe, Zn, Cu, and N-acetylneuraminic acid, as indices of the APR, were induced by these treatments. These results indicate, therefore, that the central actions of IL1 in inducing fever and the APR are separate, and that the APR is not mediated through stimulation of thermosensitive units in the POAH.