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A moderate dose of cycloheximide does not prevent the febrile response to endotoxin but interfere with induction of pyrogenic tolerance in rabbit

100%
Kozak W., Soszynski D., Wachulec M., Szewczenko M., Bodurka M.
Journal of Physiology and Pharmacology
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1992
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tom 43
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nr 2
The purpose of the present study was to examine the effect of cycloheximide (Cx) - inhibitor of protein synthesis, on the development of pyrogenic tolerance to LPS. It has been observed that Cx at a dose of 1 mg/kg given intravenously 1 h prior to LPS did not prevent fever response, however it modified the induction of pyrogenic tolerance. It was manifested in existence of the second phase of fever after the following administrations of LPS into rabbits pretreated with Cx. In control group of rabbits the induction of pyrogenic tolerance was accompanied with decaying of the second peak of fever visible as early as the second dose of LPS.
2
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Prostaglandin D2 produced by hematopoietic prostaglandin D synthase contributes to LPS-induced fever

84%
Gao W., Schmidtko A., Wobst I., Lu R., Angioni C., Geisslinger G.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 2
145-150
A large body of evidence has implicated prostaglandin E2 (PGE2) in fever production. However, the role of PGD2 in this context is only poorly understood. We therefore determined by LC-MS/MS analyses the content of PGD2 and PGE2 in cerebrospinal fluid (CSF), plasma and lungs of rats over 5 hours after fever induction by intraperitoneal injection of lipopolysaccharide (LPS, 50 µg/kg). Both PGD2 and PGE2 were detected in CSF, plasma and lungs of saline-treated control animals. The injection of LPS evoked fever and an increase of PGE2 in the CSF, while the CSF content of PGD2 was not significantly altered. However, both PGE2 and PGD2 levels were elevated in plasma and lungs after LPS injection. Interestingly, pretreatment with a novel selective inhibitor of hematopoietic prostaglandin D synthase (H-PGDS), EDJ300520 (10-40 mg/kg p.o.), selectively and dose-dependently prevented the LPS-induced increase of PGD2 in plasma and lungs but did not affect the PGE2 content. Most remarkably, EDJ300520 pretreatment led to an hypothermic response after LPS injection during the first 3 h and prevented fever induction. These data indicate that PGD2 produced peripherally by H-PGDS essentially contributes to LPS-induced fever.
3
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Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors attenuates fever due to LPS in rats

84%
Soszynski D., Chelminiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 3
Nitric oxide (NO) has been shown to be an important mediator of febrile response to lipopolisaccharide (LPS). To clarify the role of different isoforms of NO synthase (NOS) in febrile response to immune challenge, effects of selective iNOS and nNOS inhibitors on fever to LPS were examined in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine (vL-NIO), a neuronal nitric oxide synthase (nNOS) inhibitor, and aminoguanidine hydrochloride, an inducible nitric oxide synthase (iNOS) inhibitor, were injected intracerebroventricularly at a dose of 10 µg/rat just before intraperitoneal injection of LPS at a dose of 50 µg/kg. Both inhibitors injected at a selected doses had no effect on normal day-time body temperature (Tb) and normal night-time Tb. vinyl-L-NIO and aminoguanidine injected intracerebroventricularly at a dose of 10 µg/animal suppressed the LPS-induced fever in rats. The fever index calculated for rats pretreated with v-LNIO or with aminoguanidine and injected with LPS was reduced by 43% and 72%, respectively, compared to that calculated for water-pretreated and LPS-injected rats. Whereas vL-NIO partly attenuated both phases of febrile rise in Tb, administration of aminoguanidine into the brain completely prevented fever induced by LPS. These data indicate that activation of iNOS inside the brain is not only responsible for triggering but also for maintaining of LPS-induced fever in rats. It is, therefore, reasonable to hypothesize that, activation of iNOS inside the brain is more important in fever development than activation of nNOS.
4
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A comparison of febrile responses induced by LPS from E.coli and S.abortus in unrestrained rats placed in a thermal gradient

67%
Bodurka M., Caputa M., Bodurka J.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 1
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