Inhibition of Carrageenin‐Induced Rat Paw Oedema by Catecholamines and Amine‐Depleting Drugs

The anti‐inflammatory effects of adrenaline, isoprenaline, noradrenaline, tyramine, reserpine, guanethidine and fibrinolysin ® were tested against carrageenin‐induced rat paw oedema. All the substances significantly inhibited the oedema. The inhibition by tyramine enhanced the effect of reserpine. The MAO‐inhibitor iproniazid potentiated the effect of noradrenaline and reduced the effect of reserpine. The in vivo effects of adrenaline, noradrenaline, reserpine and fibrinolysin on parameters of the plasma kinin system were investigated. Neither kininogen nor prekallikrein was influenced by any of the substances tested. The effect of noradrenaline, reserpine and guanethidine on the blood serotonin level was also investigated. Noradrenaline and guanethidine did not influence the serotonin level under experimental conditions which cause a significant reduction in the carrageenin‐induced rat paw oedema. The depletion by reserpine of the serotonin stores did not correlate with the rat paw oedema inhibition values. Nevertheless, a slight reduction in the blood concentration of serotonin after pedal injection of carrageenin might indicate a local release of the amine. Finally, plasminogen was estimated by a caseinolytic procedure in the plasma of rats injected with noradrenaline. Noradrenaline inhibited the rat paw oedema, but no reduction of the plasminogen level was observed. It was concluded that normal catecholamine stores rather than normal serotonin stores, and the application to the blood platelet serotonin, seemed essential for the development of carrageenin‐induced rat paw oedema. The fact that pretreatment with catecholamines inhibited the development of oedema might suggest that the same pathway of biochemical events is involved in the inflammatory process and in the preventive mechanism, the inhibition then reflecting an acute activation and depletion of a factor later in the sequence.