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Blockade of prostaglandin E1 hyperthermia by sodium salicylate given into the ventral septal area of the rat brain.
Author(s) -
Alexander S J,
Cooper K E,
Veale W L
Publication year - 1987
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1987.sp016451
Subject(s) - sodium salicylate , hyperthermia , prostaglandin , prostaglandin e1 , chemistry , sodium , cerebrospinal fluid , medicine , endocrinology , prostaglandin e2 , prostaglandin e , ventricle , prostaglandin antagonist , blockade , pharmacology , anesthesia , receptor , organic chemistry
1. Sodium salicylate (30.0 micrograms microliter‐1) or artificial cerebrospinal fluid (ACSF) was infused bilaterally into the ventral septal area (v.s.a.) of the unrestrained rat for 1 h before and 1 h after the injection of prostaglandin E1 at a concentration of 20.0 ng microliter‐1 into a lateral cerebral ventricle. 2. During control (ACSF) infusions, 200.0 ng of prostaglandin E1 evoked a hyperthermic response (0.95 +/‐ 0.16 degrees C). During sodium salicylate infusions, the prostaglandin E1‐evoked hyperthermia was significantly reduced (P less than 0.025) to 0.31 +/‐ 0.16 degrees C. 3. The fever index (degrees C h for 1.0 h) during the infusion of sodium salicylate was reduced 66% below that of control infusions (P less than 0.01). 4. These data indicate that sodium salicylate infused in the v.s.a. of rats can antagonize a prostaglandin E‐evoked hyperthermia. This suggests that there may be an additional mechanism of action for sodium salicylate antipyresis other than inhibition of prostaglandin E synthesis.