Understanding of the antiinflammatory actions of nonsteroidal drugs is incomplete, but these actions are believed to occur in the periphery, without any contribution from the central nervous system. Recent research on the
antipyretic antiinflammatory
neuropeptide alpha-melanocyte-stimulating hormone indicates that it can act centrally to inhibit peripheral
inflammation; this raises the possibility that other agents, such as nonsteroidal antiinflammatory drugs, may have similar activity. In the present research both
lysine acetylsalicylate and
sodium salicylate inhibited
edema, induced in the mouse ear by topical application of
picryl chloride, when injected into the lateral cerebral ventricle. This inhibitory activity on a measure of acute
inflammation was not due to escape of the drugs into the periphery, because systemic injection of doses that were effective centrally did not affect
inflammation. In contrast, central administration of a dose of
indomethacin that was antiinflammatory when given intraperitoneally did not inhibit peripheral
inflammation. Thus
indomethacin apparently lacks the central antiinflammatory action of the
salicylates. This observation, plus our inability to demonstrate either an antiinflammatory effect of intracerebroventricular
dexamethasone, a
prostaglandin inhibitor, or a pro-inflammatory influence of
prostaglandin E2, suggests that
prostaglandins are not important to central modulation of
inflammation. The results indicate that, in addition to having central influences on
fever and
pain,
salicylates can act within the brain to inhibit acute
inflammation in the periphery.