W. Uhl et al., PATHOPHYSIOLOGICAL ROLE OF SECRETORY TYPE-I AND TYPE-II PHOSPHOLIPASE-A(2) IN ACUTE-PANCREATITIS - AN EXPERIMENTAL-STUDY IN RATS, Gut, 40(3), 1997, pp. 386-392
Background-In human acute pancreatitis two different types of secretor
y phospholipase A(2) (PLA(2)) have been found. Aim-To analyse the spec
ific pattern of distribution of these PLA(2) activities and their path
ophysiological role in experimental acute pancreatitis. Subjects and M
ethods-Catalytic activities of secretory type I (pancreatic) and type
II (non-pancreatic) PLA(2) and the protein concentration of immunoreac
tive pancreatic PLA(2) (IR-PLA(2)) in serum and pancreatic tissue of r
ats with cerulein (mild form) and sodium taurocholate (severe form) in
duced acute pancreatitis were determined. Results-Cerulein infusion ca
used a significant increase in type I PLA(2) activity (p<0 . 01) and I
R-PLA(2) protein concentration (p<0 . 01) in serum and pancreas, where
as type II PLA(2) activity remained unchanged during the 12 hour obser
vation period. Histology showed no significant tissue destruction. In
sodium taurocholate induced acute pancreatitis type II PLA(2) activity
significantly increased, reaching values over 10-fold higher than con
trols (p<0 . 01), whereas IR-PLA(2) protein concentration and type I P
LA(2) activity were only marginally increased. In this severe model of
acute pancreatitis significantly lower values were detected than in t
he control pancreas (p<0 . 002) for PLA(2) activity and IR-PLA(2) prot
ein concentration. Histology showed parenchymal and fat necroses with
haemorrhage, oedema, and inflammatory cell infiltration. Conclusions-T
ype I PLA(2) activity is dependent on the IR-PLA(2) protein concentrat
ion in serum and pancreatic tissue. The type II PLA(2) activity is not
stimulated by cerulein, which indicates an extra-acinar origin of thi
s enzyme. Type II PLA(2) activity is significantly increased in sodium
taurocholate induced acute pancreatitis indicating its role in the lo
cal necrotising process and involvement in the systemic effects in sev
ere acute pancreatitis.