PROSTANOIDS AND OXYGEN-FREE RADICALS IN EARLY STAGES OF EXPERIMENTAL ACUTE-PANCREATITIS

The aim of this work is to establish a relationship between prostanoid s and oxygen free radicals in the early stages of acute pancreatitis i nduced by sodium taurocholate and to study the possible cytoprotective effects of exogenous prostaglandin administration. Tissue prostanoid production (6-keto-prostaglandin F-1 alpha, thromboxane B-2, and prost aglandin E(2)) was studied after induction of an acute pancreatitis by intraductal administration of 3.5% sodium taurocholate (0.1 ml/100 mg ). The effect of previous administrations of 16,16-dimethyl prostaglan din E(2) (0.5 mu g/kg), indomethacin (20 mg/kg), or superoxide dismuta se (13 mg/kg) was evaluated. Early pancreatitis induced significant in creases of the three prostanoid levels as soon as 5 min after taurocho late administration. The administration of 16,16-dimethyl prostaglandi n E(2) was able to maintain the tissue prostanoid production at basal levels while superoxide dismutase treatment only partially prevented t he increase of 6-keto-prostaglandin F-1 alpha. On the other hand, indo methacin pretreatment, as expected, prevented the taurocholate-induced early prostanoid biosynthesis but increased the mortality, suggesting that endogenous prostanoids play a role in cellular defense mechanism s. The effect of superoxide dismutase suggests that oxygen free radica ls are responsible, in part, for prostanoid enhanced biosynthesis in t he earlier stages of necrohemorrhagic pancreatitis.