Hepatic damage during acute pancreatitis in the rat

We studied the alterations in the metabolism of liver mitochondria in rats with acute pancreatitis. Male Wistar rats were allocated to a control group (group I) and to five other groups corresponding to 2, 4, 12, 24 and 48 h after the induction of acute pancreatitis by the injection of 5% sodium tau...

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Main Authors: A.M.M. Coelho, M.C.C. Machado, S.N. Sampietre, K.R.M. Leite, V.L.L. Oliveira, H.W. Pinotti
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 1997-08-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000800006
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author A.M.M. Coelho
M.C.C. Machado
S.N. Sampietre
K.R.M. Leite
V.L.L. Oliveira
H.W. Pinotti
author_facet A.M.M. Coelho
M.C.C. Machado
S.N. Sampietre
K.R.M. Leite
V.L.L. Oliveira
H.W. Pinotti
author_sort A.M.M. Coelho
collection DOAJ
description We studied the alterations in the metabolism of liver mitochondria in rats with acute pancreatitis. Male Wistar rats were allocated to a control group (group I) and to five other groups corresponding to 2, 4, 12, 24 and 48 h after the induction of acute pancreatitis by the injection of 5% sodium taurocholate into the pancreatic duct. Sham-operated animals were submitted to the same surgical steps except for the induction of acute pancreatitis. Mitochondrial oxidation and phosphorylation were measured polarographically by determining oxygen consumption without ADP (basal respiration, state 4) and in the presence of ADP (activated respiration, state 3). Serum amylase, transaminases (ALT and AST) and protein were also determined. Ascitic fluid, contents of amylase, trypsin and total protein were also determined and arterial blood pressure was measured in all groups. In ascitic fluid, trypsin and amylase increased reaching a maximum at 2 and 4 h, respectively. Serum amylase increased at 2 h reaching a maximum at 4 h. Serum transaminase levels increased at 12 and 24 h. After 2 h (and also 4 h) there was an increase 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 mitochondrial function, which recovered after 12 h. In the 48-h groups there was mitochondrial damage similar to that occurring in ischemic lesion. Beat-to-beat analysis (30 min) showed that arterial blood pressure remained normal up to 24 h (111 ± 3 mmHg) while a significant decrease occurred in the 48-h group (91 ± 4 mmHg). These data suggest biphasic damage in mitochondrial function in acute pancreatitis: an initial uncoupled phase, possibly secondary to enzyme activity, followed by a temporary recovery and then a late and final dysfunction, associated with arterial hypotension, possibly related to ischemic damage.
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spelling doaj.art-20845675db7f4800ad588141e2c5efe82022-12-21T23:32:29ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X1414-431X1997-08-0130894795310.1590/S0100-879X1997000800006Hepatic damage during acute pancreatitis in the ratA.M.M. CoelhoM.C.C. MachadoS.N. SampietreK.R.M. LeiteV.L.L. OliveiraH.W. PinottiWe studied the alterations in the metabolism of liver mitochondria in rats with acute pancreatitis. Male Wistar rats were allocated to a control group (group I) and to five other groups corresponding to 2, 4, 12, 24 and 48 h after the induction of acute pancreatitis by the injection of 5% sodium taurocholate into the pancreatic duct. Sham-operated animals were submitted to the same surgical steps except for the induction of acute pancreatitis. Mitochondrial oxidation and phosphorylation were measured polarographically by determining oxygen consumption without ADP (basal respiration, state 4) and in the presence of ADP (activated respiration, state 3). Serum amylase, transaminases (ALT and AST) and protein were also determined. Ascitic fluid, contents of amylase, trypsin and total protein were also determined and arterial blood pressure was measured in all groups. In ascitic fluid, trypsin and amylase increased reaching a maximum at 2 and 4 h, respectively. Serum amylase increased at 2 h reaching a maximum at 4 h. Serum transaminase levels increased at 12 and 24 h. After 2 h (and also 4 h) there was an increase 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 mitochondrial function, which recovered after 12 h. In the 48-h groups there was mitochondrial damage similar to that occurring in ischemic lesion. Beat-to-beat analysis (30 min) showed that arterial blood pressure remained normal up to 24 h (111 ± 3 mmHg) while a significant decrease occurred in the 48-h group (91 ± 4 mmHg). These data suggest biphasic damage in mitochondrial function in acute pancreatitis: an initial uncoupled phase, possibly secondary to enzyme activity, followed by a temporary recovery and then a late and final dysfunction, associated with arterial hypotension, possibly related to ischemic damage.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000800006acute pancreatitishepatic lesionmitochondria
spellingShingle A.M.M. Coelho
M.C.C. Machado
S.N. Sampietre
K.R.M. Leite
V.L.L. Oliveira
H.W. Pinotti
Hepatic damage during acute pancreatitis in the rat
Brazilian Journal of Medical and Biological Research
acute pancreatitis
hepatic lesion
mitochondria
title Hepatic damage during acute pancreatitis in the rat
title_full Hepatic damage during acute pancreatitis in the rat
title_fullStr Hepatic damage during acute pancreatitis in the rat
title_full_unstemmed Hepatic damage during acute pancreatitis in the rat
title_short Hepatic damage during acute pancreatitis in the rat
title_sort hepatic damage during acute pancreatitis in the rat
topic acute pancreatitis
hepatic lesion
mitochondria
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000800006
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AT mccmachado hepaticdamageduringacutepancreatitisintherat
AT snsampietre hepaticdamageduringacutepancreatitisintherat
AT krmleite hepaticdamageduringacutepancreatitisintherat
AT vlloliveira hepaticdamageduringacutepancreatitisintherat
AT hwpinotti hepaticdamageduringacutepancreatitisintherat