EXPERIMENTAL ACUTE-PANCREATITIS RESULTS IN INCREASED BLOOD-BRAIN-BARRIER PERMEABILITY IN THE RAT - A POTENTIAL ROLE FOR TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-6

Pancreatic encephalopathy is a severe complication of acute pancreatit is. Proinflammatory cytokines may play a role in the development of mu lti-organ failure during pancreatitis. In the present study, we measur ed the changes in the blood-brain barrier (BBB) permeability concomita ntly with the determination of serum tumor necrosis factor (TNF) and i nterleukin-6 (IL-6) levels in rats before, as well as 6, 24 and 48 h a fter the beginning of intraductal taurocholic acid-induced acute pancr eatitis. Cytokine concentrations were measured in bioassays with speci fic cell lines (WEHI-164 for TNF and B-9 for IL-6), while the BBB perm eability was determined for a small (sodium fluorescein, molecular wei ght (MW) 376 Da), and a large (Evans' blue-albumin, MW 67 000 Da) trac er by spectrophotometry in the parietal cortex, hippocampus, striatum, cerebellum and medulla of rats. The serum TNF level was significantly (P < 0.05) increased 6 and 24 h after the induction of pancreatitis, while the IL-6 level increased after 24 and 48 h. A significant (P < 0 .05) increase in BBB permeability for both tracers developed at 6 and 24 h in different brain regions of animals with acute pancreatitis. We conclude that cytokines, such as TNF and IL-6, may contribute to the vasogenic brain edema formation during acute pancreatitis. (C) 1998 El sevier Science Ireland Ltd.