In rats synthesis of some
acute phase reactants can be induced by a combination of
corticosteroids and
adrenaline. During
fever both
hormones show high plasma levels. We studied the effect of
fever induced by intra-cerebroventricular (i.c.v.) injection of
PGE2 on the
acute phase response.
Fever was continuously recorded and 24 h after induction
acute phase reactant (APR) response was measured as indicated by the rise of
alpha-macrofetoprotein (alpha M FP,
alpha 2 macroglobulin of the rat). Controls received
0.9% saline i.c.v. Controls did not develop
fever (dTmax less than or equal to 1 degree C) nor did they show significant APR response. The maximal rise in body temperature after
PGE2 (2.6 +/- 0.7 degrees C) correlated significantly with the rise in alpha M FP concentration 24 h later.
Adrenalectomy prevented the APR response completely but the magnitude of the
fever reaction remained the same (2.1 +/- 0.3 degrees C). alpha-Blockade gave a smaller
fever response but had no effect on the APR response. In alpha- and beta-blockade,
fever response was normal but no APR response was obtained. Destroying the sympathetic nerve supply to the liver with 6-OH
dopamine retarded the
fever response but again APR response was not impeded. In order to differentiate between the role of
fever as such and the effect of
PGE2 on APR synthesis, we used heat exposure to induce
hyperthermia in normal rats who showed an APR response comparable with that after i.c.v.
PGE2. Pretreatment with
sodium salicylate before inducing
hyperthermia led to a variable rise in alpha M FP.
Fever as such, without tissue injury, induces an APR response. The pathway to this effect probably involves circulating
corticosterone and
adrenaline, possibly via a beta-receptor mediated stimulation.