Amm. Coelho et al., HEPATIC DAMAGE DURING ACUTE-PANCREATITIS IN THE RAT, Brazilian journal of medical and biological research, 30(8), 1997, pp. 947-953
We studied the alterations in the metabolism of liver mitochondria in
rats with acute pancreatitis. Male Wistar rats were allocated to a con
trol group (group I) and to five other groups corresponding to 2, 4, 1
2, 24 and 48 h after the induction of acute pancreatitis by the inject
ion of 5% sodium taurocholate into the pancreatic duct. Sham-operated
animals were submitted to the same surgical steps except for the induc
tion of acute pancreatitis. Mitochondrial oxidation and phosphorylatio
n were measured polarographically by determining oxygen consumption wi
thout ADP (basal respiration, state 4) and in the presence of ADP (act
ivated respiration, state 3). Serum amylase, transaminases (ALT and AS
T) and protein were also determined. Ascitic fluid, contents of amylas
e, trypsin and total protein were also determined and arterial blood p
ressure was measured in all groups. In ascitic fluid, trypsin and amyl
ase increased reaching a maximum at 2 and 4 h, respectively. Serum amy
lase increased at 2 h reaching a maximum at 4 h. Serum transaminase le
vels increased at 12 and 24 h. After 2 h (and also 4 h) there was an i
ncrease in state 4 respiration (45.65 +/- 1.79 vs 28.96 +/- 1.50) and
a decrease in respiration control rate (3.53 +/- 0.09 vs 4.45 +/- 0.08
) and in the ADP/O ratio (1.77 +/- 0.02 vs 1.91 +/- 0.01) compared to
controls (P<0.05). These results indicate a disruption of mitochondria
l function, which recovered after 12 h. In the 48-h groups there was m
itochondrial damage similar to that occurring in ischemic lesion. Beat
-to-beat analysis (30 min) showed that arterial brood pressure remaine
d normal up to 24 h (111 +/- 3 mmHg) while a significant decrease occu
rred in the 48-h group (91 +/- 4 mmHg). These data suggest biphasic da
mage in mitochondrial function in acute pancreatitis: an initial uncou
pled phase, possibly secondary to enzyme activity, followed by a tempo
rary recovery and then a late and final dysfunction, associated with a
rterial hypotension, possibly related to ischemic damage.