0736. Role of CAMP in PAF-induced intestinal endo-and epithelial dysfunction

Methods An isolated model of the rat small bowel (1) was used. Intestines were stimulated with a 0.5 nmol PAF bolus via the mesenteric artery alone (PAF, n=5) or after pretreatment with IBMX (100μM) and forskolin (0.5μM) for 20 min (PAF+PDE/AC, n=4) to increase intracellular cAMP by inhibition of phosphodiesterase (PDE) and stimulation of adenylate cyclase (AC). The pressure responses, the vascular fluid loss and the transfer of FITC-labeled vascular dextran were monitored. cAMP was measured in PAF stimulated and untreated intestines (n=5) 3 min after PAF-stimulation or at the equivalent time point.