STUDIES ON THE ACUTE INFLAMMATORY RESPONSE. I. INVOLVEMENT OF THE CENTRAL NERVOUS SYSTEM IN CERTAIN MODELS OF INFLAMMATION

¹ Mead Johnson Research Center, Evansville, Indiana

The effects of narcotic analgesics and spinal transections have been examined in formalin, carrageenin and serotonin edemas in rat paws. Serotonin edema is only slightly inhibited by spinal sectioning or narcotic analgesics. The early phase of carrageenin or formalin edema cannot be induced in spinal rats. In rats in which the hind paws have been acutely or chronically denervated, only the late phase of formalin edema can be observed. Similarly, a delayed edema does develop in spinal rats 20 to 24 hr postformalin, as in hind paws that have been acutely or chronically denervated. Normal inflammation, including the early phase, is obtained with formalin in fore paws of animals above the level of midspinal sectioning. Centrally active narcotics inhibit primarily the early phase of edema induced by formalin or carrageenin, and this action correlates with analgesic dosage. The antiinflammatory action of morphine is reversed by nalorphine but not by a beta adrenergic blocking agent, sotalol (MJ 1999; 4-(2-isopropylamino-1-hydroxyethyl)methanesulfonanilide hydrochloride). Morphine is ineffective in spinal or sham rats when given after formation of edema is well under way, and is inactive locally. Moreover, local anesthetics attenuate the inflammatory response when administered with formalin. ACTH (corticotropin) is ineffective in inhibiting the early phase of formalin edema, as are most corticosteroid-like drugs.

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