Dexamethasone pre-treatment is antipyretic toward polyinosinic: polycytidylic acid, lipopolysaccharide and interleukin 1/endogenous pyrogen

Author(s):  
H. Abul ◽  
J. Davidson ◽  
A.S. Milton ◽  
D. Rotondo
2013 ◽  
Vol 190 (8) ◽  
pp. 4103-4115 ◽  
Author(s):  
Haesun Park ◽  
Lauren Adamson ◽  
Tae Ha ◽  
Karl Mullen ◽  
Shoko I. Hagen ◽  
...  

1988 ◽  
Vol 254 (4) ◽  
pp. R633-R640 ◽  
Author(s):  
A. Morimoto ◽  
T. Nakamori ◽  
T. Watanabe ◽  
T. Ono ◽  
N. Murakami

To distinguish pattern differences in experimentally induced fevers, we investigated febrile responses induced by intravenous (IV), intracerebroventricular (ICV), and intra-preoptic/anterior hypothalamic (POA) administration of bacterial endotoxin (lipopolysaccharide, LPS), endogenous pyrogen (EP), human recombinant interleukin-1 alpha (IL-1), and prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha). Intravenous LPS, EP, or IL-1 in high concentrations caused biphasic fever. In low concentrations, they induced only the first phase of fever. Latency to onset and time to first peak of fever induced by IV injection of LPS or EP were almost the same as those after ICV or POA injection of PGE2. Fever induced by ICV or POA administration of LPS, EP, IL-1, or PGF2 alpha had a long latency to onset and a prolonged time course. There were significant differences among the latencies to fever onset exhibited by groups that received ICV or POA injections of LPS, EP, or PGF2 alpha and by groups given IV injections of LPS or EP and ICV or POA injections of PGE2. Present observations indicate different patterns of fever produced by several kinds of pyrogens when given by various routes. These results permit us to consider the possibility that there are several mediators or multiprocesses underlying the pathogenesis of fever.


1984 ◽  
Vol 246 (6) ◽  
pp. R994-R999 ◽  
Author(s):  
J. M. Krueger ◽  
J. Walter ◽  
C. A. Dinarello ◽  
S. M. Wolff ◽  
L. Chedid

When infused into the lateral cerebral ventricles of rabbits, human endogenous pyrogen (EP) preparations induced dose-dependent increases in slow-wave sleep concomitant with increasing body temperature. Heating EP to 70 degrees C destroyed its sleep-promoting and pyrogenic activity. Anisomycin (an antipyretic) prevented EP from increasing body temperature without affecting its sleep-promoting activity. Intravenous injection of EP induced fever and transient increases in slow-wave sleep but failed to induce prolonged increases in slow-wave sleep. We conclude that the somnogenic activity of EP is not secondary to its pyrogenic activity.


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