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

Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.
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PMID:Acute hemorrhagic pancreatitis in the dog. 5. The effect of antidiuretic hormone on pancreatic exocrine secretion. 59 24

A closed duodenal loop was created by the obstruction of the duodenum on either side of the common bile duct. Acute haemorrhagic pancreatitis developed within 24 h with interlobular oedema, marked acinar cell necrosis, intra-abdominal fat necrosis and ascites. Plasma amylase activity was greatly increased together with a marked decrease in albumin. There was a temporary abnormality of liver function tests due to obstruction of bile. When the duodenal obstruction was released and the animals allowed to survive there was at 3 weeks a marked reduction in the pancreatic acinar cells with fibrosis and areas of necrosis and chronic inflammatory cell infiltration. Plasma amylase activity was normal but there was an increase in total plasma protein at 3 weeks. This technique of a closed duodenal loop in the rat gives a simple, reliable and economic experimental model for studies on acute and chronic fibrotic pancreatitis.
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PMID:Acute and chronic pancreatitis in the rat caused by a closed duodenal loop. 73 44

Acute haemorrhagic pancreatitis was induced in greyhound dogs by a bile salt/trypsin injection into the main pancreatic duct. Prostaglandin-like activity in the pancreatic venous blood, right atrial blood, and arterial blood was measured by bioassay. Activity rose significantly in the pancreatic venous blood of test dogs but not in controls. Chromatographic analysis of the peritoneal exudate from the dogs with pancreatitis showed high levels of prostaglandin E-like material (mean 43 ng/ml prostaglandin E2 equivalents). It seems likely that prostaglandins contribute to the induced pancreatitis.
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PMID:Prostaglandin release in canine acute haemorrhagic pancreatitis. 126 76

Acute hemorrhagic pancreatitis was experimentally induced in the dog by the closed-duodenal-loop technique. The disease process was modified and partially reversed by intravenous infusions of vasopressin, as indicated by some of our tests for pancreatitis as well as histologic examination of the pancreas.
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PMID:Acute hemorrhagic pancreatitis in the dog. IV. Treatment with vasopressin. 127 20

Acute hemorrhagic pancreatitis was induced in Wistar rats using a retrograde intraductal injection of 5% Na-taurocholate. Rats were sacrificed at 1, 3, 6, and 24 h. Malondialdehyde and sulfhydryl groups concentration, as well as superoxide dismutase and catalase activity were measured in pancreatic, liver, and lung tissue. These parameters, with the exception of catalase, were also determined in serum and peritoneal exudate. Early and profound oxidative stress in each organ was evidenced by marked increases in malondialdehyde concentrations along with marked reductions in levels of sulfhydryl groups and superoxide dismutase; a paradoxical increase in catalase activity, perhaps compensatory, was noted in pancreas and lung. Survival for 24 h was associated with restoration of normality insofar as tissue malondialdehyde concentrations were concerned, but pancreas sulfhydryl groups remained markedly depleted. These data endorse the suggestion that the early provision of such compounds may help to accelerate recovery from hemorrhagic pancreatitis in humans.
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PMID:Oxidative stress. An early phenomenon characteristic of acute experimental pancreatitis. 128 14

The present studies were done to evaluate the therapeutic potential of several antioxidants and free radical scavengers in three different models of acute pancreatitis. (a) Edematous pancreatitis with acinar cells necrosis was induced by seven hourly intraperitoneal injections of 50 micrograms of caerulein per kg in mice. (b) Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet in mice. (c) Hemorrhagic pancreatitis was induced by retrograde infusion of 0.6 ml of 5% sodium taurocholate into the pancreatic duct in rats. The following antioxidants and free radical scavengers were given at various doses intravenously, subcutaneously, or intraperitoneally before the onset of pancreatitis: Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], superoxide dismutase, catalase, deferoxamine (Desferal), dimethyl sulfoxide, or allopurinol. The severity of pancreatitis was assessed at various times after its onset by determination of serum amylase and pancreatic weight (edema), by grading of histological alterations, and by determination of survival (survival determined in models of hemorrhagic pancreatitis). In general, free radical scavengers and antioxidants ameliorated edema and inflammation to a greater degree than necrosis and the increase in serum amylase. Superoxide dismutase (as did Ebselen in previous studies) exerted beneficial effects on survival in diet-induced pancreatitis in the absence of marked effects on pancreatic necrosis, suggesting that these beneficial effects are due to amelioration of extrapancreatic complications that often contribute to mortality in acute pancreatitis. None of the antioxidants had major beneficial effects in taurocholate-induced hemorrhagic pancreatitis. Thus, formation of free radicals may be important for progression and outcome in diet-induced and, to a lesser degree, in caerulein-induced pancreatitis but not at all in taurocholate-induced pancreatitis. Different models of pancreatitis may, therefore, involve different degrees and mechanisms of free radical formation. Despite the amelioration of edema and the beneficial effects on mortality seen for some antioxidants in some of the models, antioxidants and free radical scavengers appear to have only a limited potential for treatment of acute pancreatitis.
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PMID:Effects of antioxidants and free radical scavengers in three different models of acute pancreatitis. 164 91

Hemorrhagic pancreatitis was induced in cats by perfusing pancreatic enzymes through a pancreatic duct after the administration of intragastric ethanol. Dimethyl prostaglandin E2 was administered concurrently. In the first study, dopamine's antiinflammatory effect on the pancreas was determined in the presence of haloperidol, propranolol, or both. Next, dopamine's effects on blood flow in the normal and inflamed pancreas were compared using a hydrogen gas-clearance technique. In the final study, the effect of dopamine on fluorescein isothiocyanate-labeled dextran leakage from the pancreatic duct to portal venous blood was investigated. It was found that blockade of either dopamine or beta-adrenergic receptors reduced, and blockade of both receptors completely eliminated, the antiinflammatory effect. Dopamine had no effect on pancreatic blood flow in normal cats. In pancreatitis, although dopamine transiently reduced blood flow, after an hour flow had returned to normal. Dopamine reversed the leakage of fluorescein isothiocyanate-labeled dextran from the pancreatic duct caused by ethanol and by ethanol and prostaglandin E2. It was concluded that dopamine ameliorated pancreatitis by reducing pancreatic ductal and/or microvascular permeability rather than by altering pancreatic blood flow. The antiinflammatory effect was mediated by both dopamine and beta-adrenergic receptors.
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PMID:The antiinflammatory effect of dopamine in alcoholic hemorrhagic pancreatitis in cats. Studies on the receptors and mechanisms of action. 165 48

The purpose of this study was to investigate whether stress plays a role, morphologically and enzymatically, in the development of severe pancreatitis in rats. Acute hemorrhagic pancreatitis was induced by two intraperitoneal injections of cerulein (40 micrograms/kg body wt) at intervals of 1 h under water-immersion stress for 5 h, whereas water-immersion stress alone did not induce any morphologic and enzymatic changes in the pancreas. In this model, hemorrhagic pancreatitis developed continuously, and the serum amylase level and activation of zymogen proteases in pancreatic tissue were significantly higher than in cerulein-induced pancreatic tissue 5 h after the first cerulein injection. Furthermore, the effects of cerulein on the serum amylase level and activation of zymogen proteases were dose related. Even 5 micrograms/kg body wt of cerulein, which did not induce any evident edematous change in the pancreas, could activate the zymogen proteases of pancreatic tissue fairly well under water-immersion stress compared with pancreatitis induced by 40 micrograms/kg body wt of cerulein alone. These results indicate that stress accelerates the activation of zymogen proteases induced by cerulein and suggest the possibility that stress may play some role in the development of severe pancreatitis.
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PMID:Does stress play a role in the development of severe pancreatitis in rats? 169 53

This study evaluated the effects of the seleno-organic substance Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one] in two models of acute hemorrhagic and acute edematous pancreatitis. Ebselen is known to catalyze glutathione peroxidase-like reactions and to inhibit lipid peroxidation. Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet to mice for 66 h. Edematous pancreatitis was induced by 7-h subcutaneous injections of 50 micrograms/kg of cerulein in mice. Ebselen was given from the beginning of the CDE diet either as a subcutaneous injection of 100 mg/kg at 6-h intervals or was mixed in with the CDE diet to yield a daily dose of 100 mg/kg of Ebselen. In further experiments, Ebselen was given at various time intervals after the beginning of the CDE diet as subcutaneous injections of 100 mg/kg at 6-h intervals. In the cerulein model, Ebselen was given 5 min prior to each cerulein injection at doses from 10-500 mg/kg. Prophylactic administration of Ebselen given orally or subcutaneously significantly improved survival from 38.5% in the control group of saline-injected CDE-fed mice to 61.9 and 65.0%, respectively. Ebselen also reduced increases in serum amylase and pancreatic weight in the diet model. Therapeutic administration of Ebselen significantly increased survival only when injections were started 20 h after the beginning of the CDE diet (64%), but not when started after 40 h (44%). Similarly, increases in serum amylase and pancreatic weight due to the CDE diet were significantly reduced by Ebselen only when injections were started after 20 h but not when started after 40 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of the seleno-organic substance Ebselen in two different models of acute pancreatitis. 171 72

Acute haemorrhagic pancreatitis was induced in rats by injecting 5% sodium taurocholate into the common biliopancreatic duct. The condition was associated with an increase in the serum amylase levels as well as progressive pancreatic necrosis resulting in 100% mortality before 36 hours. This experimental model was documented by quantifying nine different parameters of pancreatic necrosis and giving more information about the induced lesion. The extent of pancreatic necrosis was evaluated at different intervals, 5.77% at 12 hours, 14.9% at 24 hours, and the rats died before 36 hours of pancreatitis induction with an average percentual necrosis of 29.9%. This model seems suitable for more pathogenic as well as therapeutic studies on acute pancreatitis in the rat.
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PMID:[Experimental acute pancreatitis in the rat. The quantification of pancreatic necrosis after the retrograde ductal injection of sodium taurocholate]. 175 Oct 64


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