Hyperthermic effects of arachidonic acid, prostaglandins E2 and F2α in rats
- Cite this article as:
- Splawinski, J.A., Górka, Z., Zacny, E. et al. Pflügers Arch. (1978) 374: 15. doi:10.1007/BF00585692
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The aim of the present study was to investigate the possibility that endotoxin fever in rats is mediated by arachidonic acid (AA) which in turn is converted to the active metabolites such as prostaglandin (PG) E2, PGF2α, thromboxane A2 (TxA2), or prostacyclin (PGI2). Evidence is presented indicating that PGE2 induces, fever (not hyperthermia) by acting on the anterior hypothalamic preoptic area. Conversely, both PGF2α and AA produce mutually similar hyperthermia and there is no correlation between their microinjection sites in the diencephalon and the observed hyperthermic response. In addition, evidence is presented suggesting that involvement of other metabolites of AA, namely TxA2 and PGI2 in the mediation of endotoxin fever in rats seems unlikely. Only PGE2-induced fever is significantly similar, consistent with the parameters of this study, to endotoxin-induced fever in rats. AA-induced hyperthermia is probably brought about by increased levels of PGF2α or both PGF2α and PGE2 in the hypothalamus following AA injection. It seems highly unlikely that endotoxin produces fever in rats through the mcreased availability of free AA or through the activation of the PG endoperoxide synthetase in the hypothalamus. The mechanism by which endotoxin may increase PGE2 levels in the rat hypothalamus remains unknown.