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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 oxygen-derived free radicals in the pathogenesis of acute pancreatitis was studied in a new model of acute hemorrhagic pancreatitis and cerulein-induced edematous pancreatitis in rats. Hemorrhagic pancreatitis was produced by administering two intraperitoneal doses of cerulein [40 micrograms/kg body weight (BW)] at 1-h intervals following water immersion stress applied for 5 h. Edematous pancreatitis was induced by injecting cerulein as described but without water immersion. Five hours after the first injection of cerulein, pancreatic edema and elevation of serum amylase level were more marked in the animals with hemorrhagic than with edematous pancreatitis. Five hours after the first injection of cerulein, marked hemorrhage and venous dilatation were observed only in those with hemorrhagic pancreatitis. Local pancreatic blood flow decreased to approximately 60% of control values in the animals with edematous pancreatitis, and to approximately 30% of control values in those with hemorrhagic pancreatitis. To evaluate the involvement of oxygen radicals, some rats received three intraperitoneal injections of superoxide dismutase (SOD 10,700 U/kg BW) and catalase (132,000 U/kg BW) beginning 15 min before the first injection of cerulein and repeated at 1-h intervals. No significant effect of free radical scavengers was observed on the edematous pancreatitis. However, in hemorrhagic pancreatitis, treatment with SOD and catalase completely suppressed the hemorrhage and venous dilatation of the pancreas, significantly reduced the pancreatic wet weight and the serum amylase level, and reduced the histologic alterations. However, after treatment with SOD and catalase, no differences were observed in local pancreatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of oxygen-derived free radicals in hemorrhagic pancreatitis induced by stress and cerulein in rats. 750 65

Oxygen free radicals (OFR) are postulated to play a role in the pathogenesis of acute pancreatitis. The aim of this work was to examine the role of xanthine oxidase in the generation of OFR and the activity of the endogenous defense mechanisms as reflected by pancreatic superoxide dismutase (SOD) activity in a model of edematous pancreatitis induced in rats by administration of cerulein at supramaximal doses, as well as in necrohemorrhagic model induced by intraductal administration of sodium taurocholate. Comparison between these two models of pancreatitis suggests important differences in origin and importance in the evolution of injury. In necrohemorrhagic pancreatitis OFR can be produced by xanthine oxidase activity probably associated to cell death. By contrast, in cerulein induced pancreatitis, other sources of oxygen free radicals, such as inflammatory cells, can be of more importance.
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PMID:Xanthine oxidase activation in cerulein- and taurocholate-induced acute pancreatitis in rats. 752 65

Studies in animal models suggest that oxygen radicals are important in the pathogenesis of acute pancreatitis. Cerulein, a decapeptide isolated from the skin of the frog, Hyla caerula, is closely related to the C-terminus of cholecystokinin and it is a potent stimulant of pancreatic exocrine secretion. The aim of the present study was to measure the activity of endogenous scavengers, superoxide dismutase, catalase and glutathione levels in cerulein-induced acute pancreatitis in rats. We found that the plasma amylase and ribonuclease levels in the pancreatitis group were both significantly high (p < 0.01, p < 0.05, respectively) when compared with the control group. Although superoxide dismutase and glutathione levels of pancreatic tissue were decreased significantly (p < 0.01, p < 0.01 respectively), we observed a significant increase (p < 0.01) in catalase activity in the cerulein treated group compared to the control group. Therefore, we concluded that the profound alteration of the activities of endogenous scavengers (superoxide dismutase, catalase) and glutathione depletion occurring after cerulein-induced pancreatitis seemed to be important in tissue injury and may provide the basis for successful therapy of the disease.
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PMID:The endogenous scavengers in cerulein-induced acute pancreatitis. 754 30

The purpose of this study was to determine the effect of superoxide dismutase (SOD) on canine experimental pancreatitis. Pancreatitis was induced by retrograde biliary juice injection (0.5 ml/kg) to accessory pancreatic duct. Twenty-one mongrel dogs were divided into two groups, i.e. control (untreated) group (n = 13) and SOD-treated group (n = 8). In SOD-treated group, SOD 5000 units/kg was administered from celiac artery immediately after onset of pancreatitis. Xanthine oxidase (XOD), malondialdehyde (MDA), phospholipase (PL), and SOD were assayed from pancreatic tissue 1 and 3 hours after onset of pancreatitis. Serum amylase, elastase I, calcium, and WBC were assayed for 7 days after onset of pancreatitis. XOD and MDA levels were increased in untreated group, and not significantly changed in treated group with statistical difference. PL levels were increased after onset of pancreatitis in both groups and SOD levels were not changed even in treated group. No statistical difference was seen in PL and SOD levels between two groups. Increase of XOD levels suggests continuous generating of free radical species from pancreatic tissue, and SOD inhibits this increase. Increase of PL level was not improved by SOD. Serum laboratory findings and survival rates were not improved by SOD treatment.
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PMID:[Role of free radicals on canine bile-induced pancreatitis and effect of superoxide dismutase]. 766 54

Effect of the complex of antiradical enzymes (superoxide dismutase and catalase in proportion 1:3) was studied on the experimental mode of acute pancreatitis. After thrice repeated administration of a complex of enzymes, antioxidant capacity of the blood serum normalized, activity of the enzymes of antioxidant protection of an organism and that of glucose-6-phosphate dehydrogenase increased, concentration of extra-erythrocytic hemoglobin decreased, contributing to normalization of morphologic structure of the pancreas in 52% of the animals with hemorrhagic and in 70%--with oedematous form pancreatitis. The results obtained are indicative of possible correction of the changes in inflammatory process in the pancreas.
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PMID:[Use of anti-radical protection enzymes in the treatment of acute experimental pancreatitis]. 793 64

The aim of this work is to establish a relationship between prostanoids and oxygen free radicals in the early stages of acute pancreatitis induced by sodium taurocholate and to study the possible cytoprotective effects of exogenous prostaglandin administration. Tissue prostanoid production (6-keto-prostaglandin F1 alpha, thromboxane B2, and prostaglandin E2) was studied after induction of an acute pancreatitis by intraductal administration of 3.5% sodium taurocholate (0.1 ml/100 mg). The effect of previous administrations of 16,16-dimethyl prostaglandin E2 (0.5 microgram/kg), indomethacin (20 mg/kg), or superoxide dismutase (13 mg/kg) was evaluated. Early pancreatitis induced significant increases of the three prostanoid levels as soon as 5 min after taurocholate administration. The administration of 16,16-dimethyl prostaglandin E2 was able to maintain the tissue prostanoid production at basal levels while superoxide dismutase treatment only partially prevented the increase of 6-keto-prostaglandin F1 alpha. On the other hand, indomethacin pretreatment, as expected, prevented the taurocholate-induced early prostanoid biosynthesis but increased the mortality, suggesting that endogenous prostanoids play a role in cellular defense mechanisms. The effect of superoxide dismutase suggests that oxygen free radicals are responsible, in part, for prostanoid enhanced biosynthesis in the earlier stages of necrohemorrhagic pancreatitis.
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PMID:Prostanoids and oxygen free radicals in early stages of experimental acute pancreatitis. 802 67

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

This paper is concerned with a hypothesis that disturbance of free radical reactions may lead to abnormality of hemorheological properties in vivo, and so the free radicals generated in vivo may damage certain tissue cells indirectly by reducing the supply of oxygen and nutrients to these cells through slowing the circulation of blood. This hypothesis is based on the following evidence: A. We have found that the whole blood viscosity at low shear rate correlates to the lipid peroxidation in the patients suffering from certain cardio- or cerebrovascular diseases, and in dogs during liver ischemia reperfusion or hemorrhagic pancreatitis. B. Reports have shown that several alterations of hemorheological properties may take place as a result of free radical reactions, such as lipid peroxidation. For instance, lipid peroxidation may lead to decrease of deformability of red cells, increase of aggregation of red cells, formation of liquid thrombin, etc. C. We have demonstrated that some alterations of hemorheological properties involve the role of free radicals in rats suffering from intestinal ischemia/reperfusion. As evidence for this conclusion, superoxide dismutase (SOD) used as a specific scavenger of superoxide anion radical (O2-) can significantly prevent the intestinal ischemia/reperfusion induced changes of lipid peroxidation, red cell aggregation, Cassion's viscosity and whole blood viscosity at low shear rate in rats.
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PMID:A new hypothesis about the relationship between free radical reactions and hemorheological properties in vivo. 818 28

We investigated microcirculatory changes in sodium taurocholate (ST)-induced pancreatitis. Groups of rats received as tracer either fluorescein isothiocyanate-dextran or acridine orange intravenously. The microcirculation of the exposed pancreas was observed by use of a video camera attached to an epi-illumination microscope. Vessel diameters and plaques of adherent leukocytes were measured with a digital image-analyzing system. In contrast to 0.4 ml of saline, intraductal infusion of ST (4%, 0.4 ml) induced a constriction of interlobular pancreatic arteries of 79 +/- 2% (P < 0.01) within 2 min. This constriction could not be antagonized by the leukotriene antagonist CGP-35949B. The radical scavengers superoxide dismutase (SOD) and N-(2-mercaptopropionyl)glycine (MPG) prevented the arterial constriction. Constriction of pancreatic arteries was accompanied by a decrease of erythrocyte velocity in the pancreatic capillaries. Flux in the head of the pancreas measured by laser-Doppler velocimetry decreased from 300 +/- 69 to 74 +/- 23 perfusion units (P < 0.01) after 446 +/- 159 s. Subsequently an increase of perfusion values was observed indicating reperfusion phenomena. ST induced leukocyte adherence to the walls of interlobular veins forming plaques constituting 39% of the observed venular cross section within 6 min. The leukotriene antagonist, SOD, or MPG prevented leukocyte adherence. Arterial constriction followed by ischemia-reperfusion and leukocyte adherence to venular endothelium during the reperfusion period represented the sequence of microcirculatory changes in ST-induced pancreatitis. The radical scavengers SOD and MPG prevented arterial constriction and leukocyte adherence to venular endothelium, indicating the involvement of free radicals in the pathogenesis of ST-induced pancreatitis in the rat.
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PMID:Arterial constriction, ischemia-reperfusion, and leukocyte adherence in acute pancreatitis. 833 66

Rats develop acute pancreatitis when infused iv for 3 h with cerulein (10 micrograms/kg/h). Autopsies of the pancreas seen by light microscope show interstitial edema, acinar cells vacuolization, and leukocyte margination in pancreatic capillaries; under electron microscope, severe damage concerning mitochondrial and zymogen granules structures are apparent. Particularly, swelling of the mitochondria and disruption of mitochondrial cristae was observed as well as formation of large vacuoles arising from zymogen granules and liposome fusion. A significant increase of lipid hydroperoxide level in the pancreatic tissue was observed. The purpose of this study was to evaluate the effect of 4-hydroxy-TEMPO--a low-mol-wt superoxide dismutase mimic--in a rat cerulein model of acute pancreatitis, with the expectation that free radical mediated hydroperoxide formation and tissue damage may be reduced significantly. Twenty-one male Wistar rats were divided into three groups: Group 1 (n = 5) served as a control and was infused iv for 3 h with physiologic saline; Group 2 (n = 8) was infused i.v. for 3 h with cerulein 10 micrograms/kg/h; and Group 3 (n = 8) infused i.v. both with cerulein and 4-hydroxy-TEMPO 22.6 mg/kg/h. Pancreatic tissue damage was quantified by measuring lipid hydroperoxide (LOOH) level, the weight of the organ, and by light and electron microscopic examination. 4-hydroxy-TEMPO penetration across cellular membrane barriers was quantified by ESR spectrometric measurements of 4-hydroxy-TEMPO concentration in pancreatic tissue samples and pancreatic juice as well. Administering 4-hydroxy-TEMPO to rats resulted in preventing both lipid hydroperoxide formation and severe morphological damage. 4-hydroxy-TEMPO crossed cellular membrane barriers and was excreted to pancreatic juice. Infusion of 4-hydroxy-TEMPO appears to prevent pancreatic injury caused by free radicals in experimental cerulein pancreatitis.
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PMID:Protective effect of 4-hydroxy-TEMPO, a low molecular weight superoxide dismutase mimic, on free radical toxicity in experimental pancreatitis. 853 Aug 31


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