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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of free radicals in the development of cerulein-induced pancreatitis was evaluated by measuring the activity of the endogenous scavengers, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHpx), as indicators of the defense system, and the level of lipid peroxide (LPO) in the pancreas, as an indicator of the offense system. Acute pancreatitis was induced by 5 hourly intraperitoneal administrations of cerulein (50 micrograms/kg body weight), in 0.9% NaCl, to mice. The presence of acute pancreatitis was confirmed by changes in serum amylase levels and in typical microscopical features. Regarding the changes in the levels of endogenous scavengers, the SOD level was decreased significantly from a basal level of 52.6 +/- 3.94 to 43.1 +/- 2.79 mU/micrograms DNA at 6 h (p less than 0.01) to 38.8 +/- 5.18 mU/micrograms DNA at 9 h (p less than 0.05) and to 31.7 +/- 3.10 mU/micrograms DNA at 12 h (p less than 0.01) after the first intraperitoneal cerulein injection. The CAT level also decreased significantly from a basal level of 7.80 +/- 0.27 to 5.86 +/- 0.46 mU/micrograms DNA at 9 h (p less than 0.01) and to 4.52 +/- 0.21 mU/microgram DNA at 12 h (p less than 0.01). GSHpx increased from a basal level of 6.80 +/- 0.43 to 7.58 +/- 0.50 mU/micrograms DNA at 9 h and to 10.2 +/- 0.52 mU/micrograms DNA at 12 h after the first intraperitoneal cerulein injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in lipid peroxide and oxygen radical scavengers in cerulein-induced acute pancreatitis. Imbalance between the offense and defense systems. 208 99

Acute edematous and necrotic pancreatitis have been induced in dogs with retrogradely intraductal injections of 5% hydrogen peroxide solution and sunflower-oil. The process of disease could be followed daily by a zipper sutured into the abdominal wound. In this manner the temporal changes of markers of oxygen-derived free radicals (concentrations of malondialdehyde and reduced glutathione of the excised pancreas tissue and abdominal exudate, as well as the superoxide dismutase content of the tissue) could be controlled. Light microscopic analysis was also done. In edematous pancreatitis reversible membrane lesions, in the necrotic form the irreversible damage of membranes and cells could be seen. The results obtained suggest the role of oxygen-derived free radicals in experimental acute pancreatitis.
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PMID:Oxygen-derived free radical reactions in experimental acute pancreatitis of the dog. 209 70

The mechanism of cerulein-induced acute pancreatitis may involve the production of free radicals in excess of the capacity of endogenous intracellular scavengers. These radicals destroy the cellular membranes, releasing digestive enzymes and cellular proteins into the interstitium. Thereafter, a cascade of events, including polymorphonuclear infiltration and complement activation, leads to pancreatic destruction. The present study demonstrates that superoxide dismutase and catalase reduce the ultrastructural and biochemical injury associated with cerulein-induced acute pancreatitis in rats. Pretreatment with superoxide dismutase and catalase 30 minutes before injury did not appear to be protective, presumably because the half-life of intravenous superoxide dismutase is only 6 minutes. This and similar studies suggest a potential clinical role for free radical scavengers in acute established pancreatitis.
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PMID:Superoxide dismutase and catalase: a possible role in established pancreatitis. 241 99

Scavengers of toxic oxygen reduction products have been reported to reduce the inflammatory reaction in some models of pancreatitis. In a blinded study, the effect of parenteral pretreatment with superoxide dismutase plus catalase was compared with placebo on pancreatitis induced in rats by infusion of 0.25% or 2% sodium taurocholate into the hepatopancreatic duct. The degree of inflammation was assessed by macroscopic examination of the pancreas, dry/wet weight ratios of pancreatic specimens, amylase activity in plasma and peritoneal exudate, the weight of the exudate, and its content of total protein. All parameters were indicative of a more severe inflammation in rats given the higher concentration of sodium taurocholate. The only significant effect of the superoxide dismutase plus catalase treatment was a moderate reduction of the dry/wet weight ratio, i.e., pancreatic edema, in rats given 2% sodium taurocholate. Our results indicate that toxic oxygen reduction products, available for interception by parenterally administered superoxide dismutase plus catalase, are of only minor importance in the pathogenesis of sodium taurocholate-induced pancreatitis in the rat.
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PMID:Parenteral superoxide dismutase plus catalase diminishes pancreatic edema in sodium taurocholate-induced pancreatitis in the rat. 246 Aug 55

The role of free radicals in the development of pancreatitis was evaluated by measuring the level of activities of xanthine oxidase (XOD), lipid peroxide (LPO) and superoxide dismutase (SOD). Acute pancreatitis was induced in female mice fed a choline-deficient meal containing 0.5% DL-ethionine (CDE meal). Acute pancreatitis was confirmed by the changes in serum amylase level and other typical features observed microscopically 24 h after the meal was taken. Activity of XOD was elevated significantly (p less than 0.05) from the baseline of 1.13 +/- 0.19 U/g tissue to 2.34 +/- 0.46, 2.59 +/- 0.33 and 3.46 +/- 0.70 U/g tissue, 8, 12 and 24 h, respectively, after the CDE meal. The LPO level was also increased from an undetectable amount to 1.10 +/- 0.47 nmol/ml (p less than 0.05), 1.03 +/- 0.18 (p less than 0.01) at 6 and 8 h, respectively, and then returned to an undetectable amount at 12 h. The peak level of LPO was shown at 24 h, 1.76 +/- 0.40 nmol/ml (p less than 0.01) and gradually decreased until 48 h, 1.17 +/- 0.37 nmol/ml (p less than 0.01) after the CDE meal. Changes of LPO took a biphasic pattern. SOD was decreased significantly from 47.1 +/- 3.4 mU/g tissue to 30.7 +/- 2.5, 24.8 +/- 1.7 and 20.6 +/- 1.1 mU/g tissue at 8 (p less than 0.01), 12 (p less than 0.01), and 24 (p less than 0.01) h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes of xanthine oxidase, lipid peroxide and superoxide dismutase in mouse acute pancreatitis. 247 6

In order to elucidate the role of oxygen-derived free radicals in acute pancreatitis, scavengers and an inhibitor of production of these free radicals were administered to rats with experimentally-induced acute pancreatitis. Acute reflux pancreatitis was produced by the occlusion of the common bile duct (OCD). Catalase and superoxide dismutase (SOD) were used as scavengers, and allopurinol was used as an inhibitor of production of free radicals. Six h after surgery, serum amylase, lipase, and thiobarbituric acid (TBA) reactant levels were elevated significantly, and histological changes in the pancreas, consisting of edema, inflammatory cell infiltration, and necrosis, partially around the intralobular and interlobular ducts, developed in the control rats receiving no agent. However, serum lipase and amylase levels in the rats given each agent were significantly lower (p less than 0.05) than in the controls. The histological changes in the pancreas were less marked in agent-treated rats than in untreated rats. These results suggest that oxygen-derived free radicals participate in the development of acute pancreatitis.
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PMID:The role of oxygen free radicals in experimental acute pancreatitis in the rat. 248 Sep 83

Cerulein-induced acute pancreatitis in rats is associated with a reversible lung injury that is characterized by alveolar capillary endothelial-cell injury, increased microvascular permeability, interstitial edema formation, and intraalveolar hemorrhage and fibrin deposition. The role of mediators in this injury was analyzed using gravimetric data, microvascular permeability indices, electron microscopy, and a quantitative morphometric analysis. Neutrophil depletion induced by a specific antibody was highly protective against lung injury. Interruption of the complement pathway (using low dose Naja naja cobra venom factor) also protected against lung injury. Catalase and superoxide dismutase were also protective. The iron chelator deferoxamine and the hydroxyl radical scavenger, dimethylsulfoxide, were not protective against acute lung injury. These data suggest that complement, neutrophils, and neutrophil-derived (H2O2-dependent) oxygen products mediate lung injury that occurs secondary to cerulein-induced pancreatitis. In contrast to other models of neutrophil-dependent, oxygen-radical-mediated lung injury, this lung injury does not appear to be an iron-dependent and hydroxyl-radical mediated injury. We postulate that the process of acute pancreatitis leads to complement activation followed by neutrophil recruitment, sequestration, and adherence to alveolar capillary endothelial cells. Ultimately lung injury appears to result from local endothelial-cell injury secondary to neutrophil-generated oxygen products that may be myeloperoxidase dependent.
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PMID:Neutrophil-dependent, oxygen-radical mediated lung injury associated with acute pancreatitis. 258 87

The role of reactive oxygen metabolites in extrapancreatic organ dysfunction associated with acute hemorrhagic pancreatitis was studied in dogs. Experimental pancreatitis was induced by the intraductal infusion of activated trypsin and taurocholate. Cardiac output, pulmonary and systemic blood pressure, pulmonary wedge pressure, central venous pressure, heart rate, blood gases and serum amylase were measured. Cardiac index, pulmonary and systemic vascular resistance, and the right and left stroke work were calculated. Systemic arterial and venous blood pressure and cardiac index gradually declined over 6 hr, while pulmonary mean blood pressure and pulmonary vascular resistance increased. Pretreatment of pancreatitis with catalase and superoxide dismutase prevented the rise in mean pulmonary blood pressure, moderated the rise in pulmonary vascular resistance, and decreased the rate and extent of the fall in cardiac index. These data suggest that reactive oxygen metabolites may play some role in the extraabdominal organ manifestations of acute pancreatitis.
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PMID:Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis. 279 9

Conscious rats were treated with a supramaximal dose of 5.10(-6)g.kg-1.h-1 of cerulein for periods of 3 and 12 h. In both groups of animals typical features of acute oedematous pancreatitis were proved by biochemical and histologic examinations. The most important finding of our study was the decrease of superoxide dismutase (SOD) activity in pancreatic tissue, accompanied by a slight increase of this scavenger enzyme in serum of rats stimulated with cerulein during 3 h. Parallelly, evident elevation of malondialdehyde (MDA) concentration in pancreatic tissue was noted. After the 12-h infusion of cerulein we were not able to detect any SOD activity in pancreatic tissue, whereas this activity appeared in ascitic fluid of tested animals. Further increase of MDA concentration in pancreatic tissue, in comparison with 3-h pancreatitis, was found. These data suggest that in 3-h and 12-h cerulein-induced pancreatitis the oxygen-derived free radicals mediate the increased lipid peroxidation in pancreatic tissue. We think that the depletion of the scavenger enzyme SOD may be responsible for such a disturbance of lipid metabolism.
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PMID:Oxygen-derived free radicals in cerulein-induced acute pancreatitis. 324 21

The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis has been investigated in a series of studies using an ex vivo, perfused canine pancreas preparation. Three models of experimental acute pancreatitis have been developed in this preparation: ischemic pancreatitis, gallstone pancreatitis, and alcohol-induced pancreatitis. In each model, the pancreas becomes edematous, gains weight, and the perfusate develops hyperamylasemia during the 4 hour period of perfusion. Pretreatment with the free radical scavengers superoxide dismutase and catalase significantly ameliorates these manifestations of pancreatic injury in each of the three models. The source of the free radical generation was investigated by pretreating the preparation with allopurinol, a quite specific inhibitor of xanthine oxidase. In each of the three models, this also significantly ameliorated the injury process. These experiments demonstrate that oxygen-derived free radicals, generated by activated xanthine oxidase, appear to play a central role in the pathogenesis of acute pancreatitis in these models. These findings shed light on the fundamental pathophysiology of this disease and may provide the basis for more effective therapy in the future.
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PMID:Oxygen-derived free radicals and acute pancreatitis: a review. 352 21


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