HEPATIC DAMAGE DURING ACUTE-PANCREATITIS IN THE RAT

Citation
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
Citations number
28
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
0100879X
Volume
30
Issue
8
Year of publication
1997
Pages
947 - 953
Database
ISI
SICI code
0100-879X(1997)30:8<947:HDDAIT>2.0.ZU;2-Y
Abstract
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.