Spławiński J A, Górka Z, Zacny E, Wojtaszek B
Pflugers Arch. 1978 Apr 25;374(1):15-21. doi: 10.1007/BF00585692.
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, PGF2alpha, 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 PGF2alpha 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 PGF2alpha or both PGF2alpha and PGE2 in the hypothalamus following AA injection. It seems highly unlikely that endotoxin produces fever in rats through the increased availability of free AA or through the activation of the PG endoperoxide synthetase in the hypothalamus. The mechanism by which endotoxin may increase PGF2 levels in the rat hypothalamus remains unknown.
本研究的目的是探究大鼠内毒素发热是否由花生四烯酸（AA）介导，而花生四烯酸又依次转化为活性代谢产物，如前列腺素（PG）E2、PGF2α、血栓素A2（TxA2）或前列环素（PGI2）。现有证据表明，PGE2通过作用于下丘脑视前区前部诱导发热（而非体温过高）。相反，PGF2α和AA均产生相互类似的体温过高，且它们在间脑的微量注射部位与观察到的体温过高反应之间无相关性。此外，现有证据表明，AA的其他代谢产物，即TxA2和PGI2参与介导大鼠内毒素发热的可能性似乎不大。只有PGE2诱导的发热与本研究的参数显著相似，与大鼠内毒素诱导的发热一致。AA注射后，下丘脑PGF2α水平升高或PGF2α和PGE2水平均升高可能导致AA诱导的体温过高。内毒素通过增加游离AA的可用性或通过激活下丘脑的PG内过氧化物合成酶在大鼠体内产生发热的可能性似乎极小。内毒素可能增加大鼠下丘脑PGF2水平的机制仍不清楚。
