Serveur d'exploration Hippolyte Bernheim

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The effect of prostaglandin E2 on the body temperature of restrained rats

Identifieur interne : 000A43 ( Main/Merge ); précédent : 000A42; suivant : 000A44

The effect of prostaglandin E2 on the body temperature of restrained rats

Auteurs : Akio Morimoto [Japon] ; Nancy C. Long [Japon] ; Tomoki Nakamori [Japon] ; Naotoshi Murakami [Japon]

Source :

RBID : ISTEX:FE4710824CB4960038F167470509E9093B5F54D8

English descriptors

Abstract

Abstract: We examined the effects of intravenous (IV) or intracerebroventricular (ICV) injection of prostaglandin E2 (PGE2) on the rectal temperature of restrained rats. The IV injection of PGE2 (0.5 mg/kg) caused hypothermia in rats with high initial rectal temperatures, but caused an elevation in rectal temperature in those animals whose starting temperatures were low. In contrast, the ICV injection of PGE2 induced fever, regardless of the rectal temperature at the time of injection. We also examined whether temperature changes due to the IV injection of endotoxin (lipopolysaccharide, LPS, 10 μg/kg) or interleukin-1β (IL-1β, 0.2 μg/kg) were dependent upon the rats' initial rectal temperatures. Rats with low rectal temperatures developed fevers in response to LPS, while animals with high starting temperatures showed hypothermia. In contrast, the IV injection of IL-1β produced fever regardless of initial rectal temperature. These data suggest that PGE2 acts centrally to cause fever and peripherally to cause hypothermia, and that following the injection of LPS, these opposing actions of PGE2 may act together to determine the thermoregulatory response.

Url:
DOI: 10.1016/0031-9384(91)90528-V

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ISTEX:FE4710824CB4960038F167470509E9093B5F54D8

Le document en format XML

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<div type="abstract" xml:lang="en">Abstract: We examined the effects of intravenous (IV) or intracerebroventricular (ICV) injection of prostaglandin E2 (PGE2) on the rectal temperature of restrained rats. The IV injection of PGE2 (0.5 mg/kg) caused hypothermia in rats with high initial rectal temperatures, but caused an elevation in rectal temperature in those animals whose starting temperatures were low. In contrast, the ICV injection of PGE2 induced fever, regardless of the rectal temperature at the time of injection. We also examined whether temperature changes due to the IV injection of endotoxin (lipopolysaccharide, LPS, 10 μg/kg) or interleukin-1β (IL-1β, 0.2 μg/kg) were dependent upon the rats' initial rectal temperatures. Rats with low rectal temperatures developed fevers in response to LPS, while animals with high starting temperatures showed hypothermia. In contrast, the IV injection of IL-1β produced fever regardless of initial rectal temperature. These data suggest that PGE2 acts centrally to cause fever and peripherally to cause hypothermia, and that following the injection of LPS, these opposing actions of PGE2 may act together to determine the thermoregulatory response.</div>
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