Abstract
Bromelain-induced edema in rats was studied and compared to carrageenin-induced edema. The edema reached a maximum 30 min after Bromelain was injected subcutaneously into the rat paw, then decreased slowly, and had almost disappeared 24 hr later. The bromelain-induced edema was obviously potentiated by the oral administration of captopril, a kininase II inhibitor, 1 hr before and after the bromelain was injected; the carrageenin-induced edema was moderately but not dose-dependently potentiated. Dexamethasone suppressed the bromelain-induced and carrageenin-induced edema, but onset of the effect was slow. Nonsteroidal acidic anti-inflammatory agents (indomethacin, piroxicam, phenylbutazone, mefenamic acid, timegadine, and benoxaprofen), except aspirin, exerted no effect on the bromelain-induced edema, whereas they significantly reduced the carrageenin-induced edema. Nonsteroidal nonacidic anti-inflammatory agents such as emorfazone, aminopyrine, tiaramide, perisoxal, and paracetamol, significantly inhibited both types of edema. Antihistamine, antiserotonin, and diuretic agents did not affect the bromelain-induced edema, but diuretic agents inhibited the carrageenin-induced edema. These results indicate that the bromelain-induced edema may be mediated mainly by bradykinin, but not by metabolites of the arachidonic acid cascade or not by biogenic amines, and that the carrageenin-induced edema is mediated predominantly by prostaglandins. The bromelain-induced edema appears to be a useful model to evaluate the effects of nonsteroidal nonacidic anti-inflammatory agents.
