Peritoneal permeability to
fluorescein-
isothiocyanate-conjugated (
FITC) dextran, mol wt 10,000 was studied in acute experimental
pancreatitis (AEP) in rats. The aim of the study was to elucidate the role of the
pancreatitis ascites and its
phospholipase A2 activity on the observed peritoneal permeability increase during AEP.
Phospholipase A2 activity of
ascites was 40 U/microL 1 h after the induction of AEP and decreased during the next 3 h gradually to a plateau of about 20 U/microL, where it remained to the end of the experiment at 24 h. A similar pattern was seen for
protein,
amylase, and
lipase although the initial peak was most pronounced for
lipase.
Pancreatitis ascites did not--irrespective of its age (1 or 20 h) or incubation time (3-20 h)--affect the peritoneal transport of
FITC dextran 10,000 in healthy rats. Similarly, intravenously-administered
ascites and intraperitoneal instillation of pancreatic
phospholipase A2 dissolved in saline were without effects. On the other hand, in another group of healthy animals,
phospholipase dissolved in fresh
pancreatitis ascites caused a statistically significant increase of peritoneal transport, as defined. In rats with
pancreatitis, the addition of
phospholipase A2 to the peritoneal fluid increased peritoneal transport of
FITC dextran 10,000 as well as
phospholipase A2 itself. We conclude that
phospholipase A2 when instilled into the peritoneal cavity in the presence of
pancreatitis ascites, has the ability to increase peritoneal permeability to
FITC dextran 10,000 in healthy, as well as in
pancreatitis rats. However, the
phospholipase A2 activity of rat
pancreatitis ascites is not sufficient for this mechanism to work. This, however, does not exclude its existence in other species, including humans.