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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes in the cellular concentrations of ATP, ADP, AMP and oxidative phosphorylation of mitochondria in the liver were investigated experimentally in rats with acute pancreatitis (AP). The energy charge (ATP + 1/2ADP)/(ATP+ ADP+ AMP) of the liver decreased from 0.866 to 0.806 (P < 0.05) at 24 hours after onset of AP, and continuously decreased to 0.769 (P < 0.01) at 48 hours. On the other hand, the mitochondrial phosphorylative activity increased rapidly to 130% and 157% in the controls at 12 hours and 24 hours respectively and then decreased rapidly at 48 hours. The blood ketone body ratios were paralleled to the hepatic energy charge level in AP rats. These findings suggest that the nature of the derangement of the hepatic energy metabolism initiated by AP is that the effects of mitochondria damage result in a significant decrease in liver energy charge level, leading ultimately to hepatocellular impairment, and the measurement of the blood ketone body ratio is useful in evaluating the energy status of the liver in AP patients.
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PMID:Changes in hepatic energy metabolism in experimental acute pancreatitis. 145 73

To evaluate the effects of acute pancreatitis on the energy metabolism of the liver and on the fragility of hepatic cells and subcellular organelles, we studies (1) the arterial blood ketone body ratio (BKBR) (aceto acetate/beta-hydroxy butyrate), which is in equilibrium with the free NAD+/NADH ratio in liver mitochondria; (2) the hepatic energy charge (EC) = (ATP + 1/2 ADP)/(ATP + ADP + AMP); (3) the cathepsin B leakage from hepatic lysosomes and the malate dehydrogenase leakage from hepatic mitochondria in vitro; and (4) the protective effects of prostaglandin E2 (PGE2) and a new synthetic protease inhibitor ONO 3307 on hepatic injury in acute pancreatitis induced in rats by a supramaximal dose of caerulein. Decreased BKBR and hepatic EC as well as increased hepatic lysosomal and mitochondrial fragility were observed in rats with this type of acute pancreatitis, and both PGE2 and ONO 3307 had a significant protective effect against hepatic injury in these rats, especially ONO 3307. These results suggest that impaired hepatic energy metabolism is closely related to increased hepatic lysosomal and mitochondrial fragility and that some proteases, which are derived from pancreatitis and are susceptible to inhibition by ONO 3307, seem to play an important pathological role in this liver injury induced by pancreatitis. Therefore, it is important to take care of the liver in patients with acute pancreatitis.
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PMID:Impaired hepatic energy metabolism in rat acute pancreatitis: protective effects of prostaglandin E2 and synthetic protease inhibitor ONO 3307. 152 49

The damage to the liver during acute pancreatitis (AP) could be partly dependent on depressive action of pancreatitis associated ascitic fluid (PAAF) on the energy metabolism of hepatocytes. The aim of the study was to assess the effect of PAAF from dogs with acute experimental pancreatitis (AEP) and from humans with AP on the respiratory function of isolated rat liver mitochondria (RLM). The mitochondrial oxygen consumption rate in state 3 respiration (with ADP) and in state 4 (without ADP) using sodium succinate as substrate and oxygen Clark's electrode was estimated. Respiratory control ratio (RCR) and P/O ratio were calculated. PAAF was collected after 6 h of AEP induced by Elliott's method in 8 dogs, and from 4 patients with AP, intraoperatively. Both animal and human PAAFs increase the oxygen consumption rate by RLM in state 4 dose dependently (by 65% with 50 microL to 150% with 200 microL of canine PAAF). This uncoupling effect of human PAAF was twice more potent than the canine. Dialysis of PAAF reduced this effect almost completely. The mitochondrial ATPase activity in RLM treated with PAAF was stimulated and this effect was also reduced by dialysis. The conclusion was that the damage to the liver in AEP could be partly dependent on the toxicity of dializable component(s) of PAAF on the energy metabolism of mitochondria. These findings may partly explain the beneficial effects of peritoneal lavage in acute pancreatitis.
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PMID:The effect of pancreatitis associated ascitic fluid on some functions of rat liver mitochondria. A possible mechanism of the damage to the liver in acute pancreatitis. 248 Sep 84

The role of blood platelets in the disturbed haemostasis in acute pancreatitis is not fully elucidated. The aim of this study was to evaluate the blood platelet function during the first hours of acute experimental pancreatitis (AEP) in dogs. AEP was induced by the retrograde injection of bile and trypsin into the main pancreatic duct. Platelet count, platelet aggregation induced with ADP, PAF, AA as well as plasma Beta-TG and TXB2 levels were determined. At 30 min after induction of AEP a significant decrease of platelet count was noted; these changes were observed until 4 th hr. At 30 min as well as at 60 min of AEP increased sensitivity of platelet aggregation to ADP was found. After that time evident decrease of platelet aggregation to ADP was shown. Platelets sensitivity to PAF was higher at 30 min of AEP whereas 60 min, 2 and 4 hrs after AEP normalization of platelet aggregation by PAF was observed. The significant increase of plasma Beta-TG and TXB2 concentrations corresponded well to changes of platelet aggregation. These results indicate that AEP affects blood platelet function with the drop of their count.
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PMID:Does acute experimental pancreatitis affect blood platelet function? 252 19

The purpose of this study was to evaluate the effect of free radical ablation therapy in acute hemorrhagic pancreatitis. Acute pancreatitis was induced in 64 rats by retrograde injection of 5% sodium taurocholate. Thirty animals were pretreated with 100,000 units/kg/hr of superoxide dismutase (SOD) and 400,000 units/kg catalase within the first 3 hr. After 0.5, 3.5, and 12 hr of observation time, serum enzymes and the tissue content of conjugated dienes, malondialdehyde, reduced and oxidized glutathione, as well as ATP, ADP and AMP were measured. In addition, tissue samples were examined by light microscopy. Untreated rats (N = 34) developed within 12 hr an acute hemorrhagic necrotizing pancreatitis with a concomitant increase in serum enzyme levels and a decrease in reduced glutathione and ATP. Within the 12-hr observation period, 57% of the animals died. Scavenger treatment improved the tissue damage and attenuated the increase of the serum enzyme levels and the decrease in reduced glutathione and ATP. Moreover, the lethality rate was significantly lower. Oxygen radicals seem to be instrumental for the development of acute hemorrhagic pancreatitis. Thereby, antioxidant treatment reduces tissue damage, biochemical alterations and extrapancreatic complications, thus improving the final outcome.
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PMID:Effect of antioxidant treatment in rats with acute hemorrhagic pancreatitis. 817 16

In order to assess the cumulative effects of antecedent acute ethanol intake and acute pancreatitis on the liver, the mitochondrial respiratory functions and lysosomal membrane integrity of the liver were evaluated in taurocholate pancreatitis (AP) in rats, induced 6 hr after intragastric ethanol 40% (5 g/kg body wt). The oxygen consumption rate, RCR (respiratory control ratio), and ADP/O ratio were measured according to Estabrook. Fractional free activity of lysosomal hydrolases was assayed. RCR with glutamate + malate was most decreased at 12 hr of AP with partial improvement after 18 hr. The ADP/O ratio dropped maximally after 18 hr of AP. The fragility of lysosomal membranes increased significantly at 18 hr of AP. The antecedent ethanol intake abolished the partial restoration of RCR after 18 hr; however, it did not affect the ADP/O ratio or the integrity of lysosomal membranes impaired in AP at this time. In conclusion, the antecedent acute ethanol abuse could aggravate the liver mitochondrial deterioration, but not the lysosomal membrane labilization seen in AP.
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PMID:Hepatic mitochondrial and lysosomal alterations in acute experimental pancreatitis with ethanolic coetiology in rats. 856 47

The damage to the liver appears to be an important aspect of multisystem organ failure in acute pancreatitis with poor prognosis. The objective of this study was to evaluate the protective effect of stable prostacyclin analogue--tilsuprost on the liver energy metabolism in taurocholate pancreatitis in rats preceded by acute ethanol intake. The respiratory control ratio (RCR) and ADP/O ratio of liver mitochondria with glutamate+malate as substrates and mitochondrial DNP (uncoupler)-dependent ATPase activity were significantly depressed after 12 h of taurocholate pancreatitis-the effects that were not significantly aggravated by antecedent acute ethanol intake. Tilsuprost (0.3 mg/kg i.g.) given just before induction of pancreatitis partly prevented the impairment of mitochondrial oxidative and phosphorylative functions, however these positive effects were limited in acute pancreatitis preceded by acute ethanol intake. These results suggest that prostacyclin analogues could be effective in the treatment of hepatic complications in acute pancreatitis, however their effectiveness could be limited in the case of acute ethanol antecedent abuse.
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PMID:The effect of tilsuprost on the liver mitochondria in taurocholate pancreatitis in rats with antecedent acute ethanol abuse. 887 59

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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PMID:Hepatic damage during acute pancreatitis in the rat. 936 23

The mechanism whereby somatostatin (SS) produces beneficial effects in established pancreatitis induced by pancreaticobiliary duct ligation (PBDL) is still not clear. The aim of the work was to evaluate the possibility of a direct action of SS on pancreatic acinar cells from rats with acute pancreatitis. For this purpose, we studied the SS-receptor-adenylate cyclase system in pancreatic acinar membranes from both, control rats and rats with experimentally induced acute pancreatitis. On the other hand, it has been reported that cholecystokinin (CCK) diminishes the number of SS receptors in pancreatic acinar cells. Proglumide, a CCK receptor antagonist reduces the severity of acute pancreatitis in the rat. Therefore, we have also examined the effect of proglumide on the somatostatinergic system in controls and rats with acute pancreatitis. Fourteen hours after PBDL, the SS receptors, the capacity of the SS analogue SMS 201-995 to inhibit forskolin-stimulated adenylate cyclase activity and PTX-catalyzed [32P] ADP-ribosylation of the alpha1 subunits of Gi proteins could not be detected in pancreatic acinar membranes. One month after reopening the closed pancreaticobiliary duct (PBD), the pancreas showed regeneration of acinar cells, and the above-mentioned parameters were significantly lower than in the control group. Two months after reopening the closed PBD, all these parameters had returned to control values. The administration of proglumide (20 mg/kg i.p.), a cholecystokinin receptor antagonist, accelerated pancreatic regeneration and approached all these parameters to control values one month after reopening the closed PBD. The present study suggests that the beneficial effects of SS on established pancreatitis induced by PBDL may not be due to a direct action of the peptide on pancreatic acinar cells at least at 14 hours after PBDL. In addition, these findings suggest that in established pancreatitis the effect of proglumide on the SS receptor-adenylate cyclase system could be due to its action on pancreatic regeneration.
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PMID:The somatostatin receptor-adenylate cyclase system in rat pancreatic acinar membranes after temporary pancreaticobiliary duct ligation. 940 49

Acute Pancreatitis (AP) is known to produce morphologic and functional changes in liver. Administration of low doses of caerulein significant decreases the content of pancreatic enzymes, leading to reduced mortality of animals submitted to AP. The present study was designed to assess the effect of acute reduction of pancreatic enzymatic content in the hepatic mitochondrial function. Wistar male rats, submitted to AP by injection of Na thaurocholate into the pancreatic duct, with and without previous i.v. injection of 0.133 microgram Kg-1h-1 of caerulein for three hours, were divided in four groups: Group I: No caerulein infusion and AP; Group II: Previous caerulein infusion and with AP; Group III: Caerulein infusion without AP; Group IV (control): No caerulein infusion and without AP. After 2 hours of induction of AP the livers were removed and prepared to the mitochondrial oxidative and phosphorylative activities, measured polarographically with determination of oxygen consumption without ADP (Basal respiration-State 4) and in the presence of ADP (Activated respiration-State 3). Ascitic fluid contents of amylase, trypsin and total protein were routinely determined. After 2 hours of AP there was a significant increase in state 4 respiration (41%) and a decrease in respiratory control ratio and in ADP/O ratio (p < 0.05) in animals of Group I (AP without caerulein) when compared to Group II (AP with caerulein) (Table 1). Ascitic fluids contents of amylase (A) and trypsin (T) showed decrease in animals of Group II with AP that received previous caerulein infusion (A = 80 +/- 10 U/ml, T = 9.75 +/- 1.25 U/ml), when compared to animals of Group I that did not receive caerulein (A = 231 +/- 24, T = 40.32 +/- 5.19) (p < 0.001). Caerulein infusion by itself (Group III) did not have any influence on mitochondrial liver dysfunction. Reduction of pancreatic enzyme content through caerulein infusion attenuates the damage of mitochondrial respiration, demonstrated by uncoupling phase on mitochondrial function in experimental AP. Further studies are needed to elucidate this phenomena, but it is probably related to the decreased of the pathogenic effects of pancreatic activated enzymes that reach the systemic circulation in reduced amounts.
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PMID:[Hepatic lesion in experimental acute pancreatitis. Influence of pancreatic enzyme storage reduction]. 1043 40


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