Massart-Leën A M, Burvenich C, Vandeputte-Van Messom G, Hilderson H
Department of Veterinary Physiology, Faculty of Veterinary Medicine, University of Ghent, Belgium.
Domest Anim Endocrinol. 1992 Oct;9(4):273-83. doi: 10.1016/0739-7240(92)90015-p.
In a first series of experiments we studied the influence of E. coli endotoxins or lipopolysaccharides (LPS) administered either intravenously (i.v.) or intramammarily (i.mam.) to lactating goats on plasma cortisol and rectal temperature (RT). Differences in the magnitude of the cortisol release and shape of the fever curve were observed. In both models maximal pyrexia and fever index (FI) were comparable. In a second series of experiments the influence of LPS on the plasma cortisol and RT was studied after i.v. injection of increasing doses of LPS:low (25 ng/kg), moderate (200 ng/kg) and relatively high (500 ng/kg). Although the cortisol response was dose dependent, the effect was not correlated with FI. The administration of flurbiprofen, a non steroidal antiinflammatory drug (NSAID), resulted in a complete inhibition of fever at all LPS doses and the cortisol release after administration of low doses LPS. This indicates a prostaglandin mediation. With moderate and high doses LPS the cortisol release was only partially inhibited and delayed suggesting a non prostaglandin mediated mechanism. In a third series of experiments the influence of flurbiprofen on fever and cortisol release was studied after i.mam. LPS administration. The observed increase of plasma cortisol and RT were completely abolished after flurbiprofen treatment. It is concluded that: 1) the increase of plasma cortisol after LPS administration in lactating goats is not related to hyperthermia per se, 2) the control of fever and cortisol release may, to some extent, differ according to the LPS dose and method of administration, 3) the cortisol release observed after moderate and high doses of LPS is probably controlled by two phenomena. The first being induced by cyclo-oxygenase metabolites, the second by intermediary mediators other than prostaglandins or by LPS itself. 4) Although an eight-fold higher dose of LPS was given i.mam., a cortisol release comparable to the lowest dose of LPS (25 ng/kg) was observed. These differences in cortisol release can be ascribed to 1) a detoxification of LPS at the level of the mammary gland or 2) a slower resorption of LPS from the mammary gland.
在第一组实验中，我们研究了静脉注射（i.v.）或乳腺内注射（i.mam.）大肠杆菌内毒素或脂多糖（LPS）对泌乳山羊血浆皮质醇和直肠温度（RT）的影响。观察到皮质醇释放幅度和发热曲线形状存在差异。在两个模型中，最大发热和发热指数（FI）相当。在第二组实验中，静脉注射递增剂量的LPS（低剂量25 ng/kg、中等剂量200 ng/kg和相对高剂量500 ng/kg）后，研究了LPS对血浆皮质醇和RT的影响。尽管皮质醇反应呈剂量依赖性，但该效应与FI无关。给予非甾体抗炎药（NSAID）氟比洛芬后，在所有LPS剂量下发热均被完全抑制，低剂量LPS给药后皮质醇释放也被抑制。这表明存在前列腺素介导作用。对于中等剂量和高剂量LPS，皮质醇释放仅被部分抑制且延迟，提示存在非前列腺素介导机制。在第三组实验中，乳腺内注射LPS后，研究了氟比洛芬对发热和皮质醇释放的影响。氟比洛芬治疗后，观察到的血浆皮质醇和RT升高被完全消除。得出以下结论：1）泌乳山羊给予LPS后血浆皮质醇升高与体温过高本身无关；2）发热和皮质醇释放的控制可能在一定程度上因LPS剂量和给药方法而异；3）中等剂量和高剂量LPS后观察到的皮质醇释放可能受两种现象控制。第一种由环氧化酶代谢产物诱导，第二种由前列腺素以外的中间介质或LPS本身诱导。4）尽管乳腺内注射的LPS剂量高八倍，但观察到的皮质醇释放与最低剂量LPS（25 ng/kg）相当。皮质醇释放的这些差异可归因于：1）乳腺水平对LPS的解毒作用；2）LPS从乳腺的吸收较慢。
