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

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

In order to investigate pancreatitis caused by cold ischemic damage to pancreatic grafts, an isolated, normothermic, ex vivo perfusion model was employed. Canine pancreases were subjected to 24 and 48 h of cold ischemia and then reperfused. The results showed that cold ischemia results in pancreatitis as measured by weight gain (tissue edema) and elevated leakage of amylase into the perfusate. The addition of allopurinol to the perfusion system did not prevent the signs of pancreatitis. From the results it can be concluded that the isolated, perfused pancreas model in the dog is useful for studying preservation-induced pancreatitis. The absence of any effect of allopurinol treatment suggests that oxygen-free radicals mediated by the xanthine oxidase system is of minor importance for the pathogenesis of postischemic pancreatitis.
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PMID:Preservation-induced pancreatitis in an isolated perfused pancreas model in the dog. 247 41

We describe our serendipitous finding of a transplantation model of hemorrhagic pancreatic necrosis. The slow evolution, from edematous interstitial pancreatitis to hemorrhagic necrosis over the course of 8 days made the model amenable to therapeutic manipulation. The possible pathogenesis is discussed with reference to the published literature. From comparisons between the histologic and biochemical features of isografts and allografts, we suggest that ischemia-reperfusion injury initiates pancreatitis through oxygen-free radicals, and that the transformation to hemorrhagic pancreatic necrosis in allografts reflects the involvement of chemotactic immune factors and extracellular secretions from activated proteases.
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PMID:Acute pancreatitis after experimental pancreatic transplantation. 247 76

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

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

In this experiment, free radicals in the pancreas of endotoxemia and ethionine induced acute pancreatitis in mice were attempted to be detected directly by ESR spectroscopy, using 77 K freeze-trapping and 25 degrees C DMPO spin trapping techniques. In the 77 K freeze-trapping method, Mn (II) ion and R-00. radical were detected in endotoxemia and ethionine induced pancreatic lesions. The heme-NO radical was observed at 6 and 24 h after isolation of the normal pancreas, and signal intensity was increased with time. This finding supports that ESR spectroscopy is a useful method for detecting the tissue degeneration process from ischemia to necrosis. Using the DMPO spin trapping technique (25 degrees C), 6-line was detected at 6 h after intraperitoneal administration of E. coli in the model of endotoxemia, and 3- and 6-lines and a signal suggestive of DMPO-OH adduct were noted at 12 and 24 h in ethionine pancreatitis. These findings suggest that impaired pancreatic tissues exist in a considerably oxidative environment and oxygen derived free radicals may be considered to play an important role in the development of pancreatic lesions.
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PMID:Direct ESR measurement of free radicals in mouse pancreatic lesions. 255 71

Recent experimental work has suggested that oxygen-derived free radicals may play an important role in initiating the early capillary injury in acute pancreatitis. Data from models of ischemic injury in other organs have suggested the enzyme xanthine oxidase is important in generating oxygen-derived free radicals. The present study was performed to determine whether xanthine oxidase is the source of free radical production in experimental pancreatitis. Utilizing the isolated, perfused, ex vivo canine pancreas preparation, three models of pancreatitis were initiated with (1) free fatty acid infusion (FFA), (2) partial duct obstruction and secretin stimulation (POSS), and (3) ischemia (ISCH). In each model, during a 4-hour perfusion, edema developed, weight gain occurred (FFA 120.6 +/- 21.1 gm; POSS 44.5 +/- 6.9 gm; ISCH 63.3 +/- 14.0 gm), and the serum amylase became elevated (FFA 1827 +/- 397 u/dl; POSS 10,171 +/- 1487 u/dl; ISCH 1860 +/- 365 u/dl). When the xanthine oxidase enzyme inhibitor allopurinol was added to the perfusate prior to the 4-hour perfusion, edema formation was absent or minimal, weight gain was significantly less (FFA 15.2 +/- 2.5 gm p less than 0.05; POSS 8.8 +/- 2.7 gm p less than 0.001; ISCH 12.3 +/- 2.8 gm p less than 0.01), and the amylase remained normal or the elevation was significantly decreased (FFA 996 +/- 189 u/dl p less than 0.05; POSS 3021 +/- 1074 u/dl p less than 0.001; ISCH 993 +/- 214 u/dl p less than 0.002). These data confirm that oxygen-derived free radicals play an important role in the pathogenesis of experimental acute pancreatitis, and suggest that the enzyme xanthine oxidase may well be the source of their production.
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PMID:The pathogenesis of acute pancreatitis. The source and role of oxygen-derived free radicals in three different experimental models. 258 19

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

Diffuse alveolar damage (DAD) is usually considered a generalized lung process. During five years the authors observed 83 patients with generalized DAD in 827 adult autopsies (10.1%) and 10 patients with identical, but localized, lesions. The authors propose the term regional alveolar damage (RAD) to designate localized "DAD." RAD was unilateral in six patients and most frequently involved the upper lobe. All ten patients had chronic systemic diseases and presented with life-threatening illnesses. The probable causes of RAD were multifactorial and included hypotensive shock, septicemia, pneumonia, hyperoxia, and pancreatitis. All patients developed respiratory failure, requiring supplemental oxygen and, in nine patients, mechanical ventilation. Chest roentgenograms revealed alveolar or combined alveolar and interstitial infiltrates that corresponded to the lesions found at autopsy. The reasons for localization of RAD within the lung are unclear, but the presence of proliferative lesions and frequent involvement of the upper lobe suggests that RAD is not simply an early phase of DAD and implicates additional pathogenetic factors.
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PMID:Regional alveolar damage (RAD). A localized counterpart of diffuse alveolar damage. 266 70

Experimental study had been conducted on 18 healthy adult mongral dogs of both sex, weighting from 7.5-11 kg, randomly divided into four groups. Experimental models of acute hemorrhagic necrotizing pancreatitis (AHNP) were established by retrograde injecting 1 ml/kg of sodium taurocholate directly into the pancreatic duct. The dogs were treated respectively with intravenous infusion of Salviae miltiorrhizae (5 g/kg), 654-2(5 mg/kg) or normal saline. The results showed that PaO2, PaCO2 and pH did not change in early stage of AHNP. The contents of lactic acid dehydrogenase (LDH), albumin and lipid peroxide (LPO) of bronchoalveolar lavage fluid in the AHNP group were significantly higher than that of Salviae miltiorrhizae group (P less than 0.05). The necrosis and disruption of conjunction of endothelial cells resulting from the defects of vascular wall were noted under transmission electron microscope. Both pulmonary vascular and type II pneumocyte were normal in the Salviae miltiorrhizae group. These results suggested that Salviae miltiorrhizae possess the effect of protecting endothelial cells of pulmonary vascular and type II pneumocyte, which could function as scavenger of oxygen-derived free radicals.
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PMID:[Protective effects of Salviae miltiorrhizae and anisodamine (654-2) against early lung injury in acute hemorrhagic necrotizing pancreatitis in the dog]. 273 1


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