Blockade of prostaglandin E1 hyperthermia by sodium salicylate given into the ventral septal area of the rat brain.

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.