Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perfusion of the pancreatic duct with acidified aspirin in cats increased the permeability of the duct to HCO3-. Intravenous administration of the synthetic prostaglandin analog 16,16 dimethyl prostaglandin E2 (PGE2) prevented this permeability change. The effect was dose-related and at the highest dose (50 microgram/kg/hour) was essentially complete. The beneficial effect of the PGE2 was apparent even when it was given after the duct had been exposed to aspirin. PGE2 had no effect on pancreatic water or electrolyte secretion in the unstimulated nonsecreting gland. No histologic changes in the pancreatic ducts were seen after exposure to aspirin, PGE2 or both. The effectiveness of PGE2 in restoring membrane permeability towards normal suggests the possibility of its therapeutic role in pancreatitis.
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PMID:Effect of 16, 16 dimethyl prostaglandin E2 on aspirin-induced permeability changes in the pancreatic duct. 745 23

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

Taurolidine has potent antiendotoxin and antimicrobial effects in vitro. This study assessed the effect of taurolidine in a well-described model of acute pancreatitis. Ninety-five male Wistar rats (250 g) were studied. Pancreatitis was induced by intraductal injection of 50 microliters of a 4% sodium taurocholate solution at a pressure of 25 cm water. Animals were randomly allocated to 1 of 10 groups: 4 groups were used to characterize the model and there were 6 treatment groups. Taurolidine (100 mg/kg) or saline was administered intravenously at Time 1, 4 hr, or 4 and 24 hr following induction of pancreatitis. Serum amylase, endotoxin levels, and blood cultures were assessed at 4 and 24 hr. Survival was documented at 1 week. Serum amylase levels were elevated in animals in whom acute pancreatitis was induced; however, there was no difference in serum amylase between animals treated with taurolidine and those treated with saline. Positive blood cultures were more numerous in saline-treated groups. Treatment with taurolidine was associated with significantly (P < 0.01) lower endotoxin levels (14 +/- 8 pg/ml) compared with saline-treated animals (350 +/- 87 pg/ml). Taurolidine administration significantly improved survival compared with controls, when given at 4, 24, and 4/24 hr postinduction of pancreatitis (P < 0.05). Taurolidine was beneficial in this model of acute pancreatitis.
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PMID:Beneficial effects of taurolidine in experimental pancreatitis. 751 18

Blockage of the rat pancreatico-biliary duct (PBDO) for 4 hours and secretin infusion (0.2 CU [Clinical Unit]/kg/hr) caused significant rises in portal serum amylase, cathepsin B levels, pancreatic water content, and pancreatic amylase content as well as lysosomal and mitochondrial fragility. Impaired pancreatic adenylate energy charge levels were also noted. These changes tended to continue for 12 hours after the release of PBDO and disappeared after 24 hours. All the changes induced by PBDO with secretin infusion were no longer observed at 48 hours. The administration of a new potent protease inhibitor, E-3123 at a dose of 5 mg/kg/hr during PBDO markedly attenuated all the parameters examined, exerting a significant protective effect on acinar cells in this model. These results indicate the important roles of subcellular organelle fragility and impaired pancreatic energy metabolism in the pathogenesis of pancreatic injuries induced by common channel obstruction with intraductal hypertension, and also indicate the possible usefulness of E-3123 in the treatment of acute pancreatitis such as gallstone pancreatitis.
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PMID:Effect of short-term pancreatico-biliary duct obstruction with intraductal hypertension on subcellular organelle fragility and pancreatic adenylate energy metabolism in rats: protective effect of a new protease inhibitor, E-3123. 751 90

Water-immersion stress is known to be involved in the development of hemorrhagic pancreatitis in caerulein-induced pancreatitis, when the stress is given following caerulein injection. The effects of pre-treatment with water-immersion to caerulein-induced pancreatitis were investigated in this study. 1. A 60-kDa heat shock protein was induced by pre-treatment with water-immersion stress in the pancreas. 2. Intra-peritoneal injection of caerulein (40 micrograms/kg) induced acute pancreatitis in rats without pre-treatment with water-immersion. However, when the rats were pre-treated with water-immersion, acute pancreatitis was not developed and no change of serum amylase levels was observed by i.p. injection of caerulein.
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PMID:Induction of heat shock protein and prevention of caerulein-induced pancreatitis by water-immersion stress in rats. 752 Mar 97

Nitric oxide (NO) has been implicated to regulate pancreatic circulation, promote capillary integrity, and inhibit leukocyte adhesion. We investigated the role of NO in the development of pancreatitis. Nitro-L-arginine, an inhibitor of NO synthase, in total dose of 35 mg/kg body wt was infused in the rats with edematous pancreatitis induced by two intraperitoneal injections of cerulein (20 micrograms/kg). L-Arginine (125 or 250 mg/kg), a NO donor was intravenously administered twice in the rats with hemorrhagic pancreatitis induced by water-immersion stress plus two intraperitoneal injections of cerulein (40 micrograms/kg). The degree of pancreas edema, serum amylase levels, and histologic alterations were investigated. Nitro-L-arginine exacerbated cerulein-induced pancreatitis and caused a decrease in pancreatic blood flow. L-Arginine ameliorated the severity of hemorrhagic pancreatitis dose dependently and improved the pancreatic blood flow. These findings suggest that NO could confer protection against the development of hemorrhagic pancreatitis, probably through improvement of the pancreatic microcirculation.
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PMID:Protective effect of nitric oxide on development of acute pancreatitis in rats. 758 83

Pancreatic infection from gut-derived bacteria has emerged as the major cause of death in necrotizing pancreatitis. Bacterial overgrowth of indigenous enteric organisms as a consequence of guts stasis (ileus) represents a potential initial event in this process. The present study was designed to examine the interrelationships between intestinal transit, enteric bacteriology, and the translocation of bacteria from the gut lumen to mesenteric lymph nodes and splanchnic viscera during experimentally induced acute pancreatitis. Male rats underwent pancreaticobiliary duct ligation (PBDL) or sham surgery and were sacrificed after 24, 48, or 96 hr. Severity of pancreatitis was assessed with histology, tissue water content, and amylase and lipase levels. Intestinal transit was measured with fluorescent tracers. Blood, mesenteric lymph nodes (MLNs), splanchnic organs, and gut luminal contents were subjected to bacteriologic analysis. PBDL was followed by biochemical and histologic evidence of progressive pancreatic injury at each time interval. Enteric bacteria within the gut and in adjacent MLNs increased as intestinal transit decreased after PBDL-induced pancreatic inflammation. Surprisingly, all parameters returned to control levels by 96 hr in spite of progression of pancreatic inflammation.
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PMID:Intestinal transit and bacterial translocation in obstructive pancreatitis. 764 83

The effects of single and repeated short-term (4 hr) obstruction of pancreaticobiliary duct (PBDO), with or without exocrine stimulation (intraductal hypertension) by cerulein infusion (0.2 micrograms/kg.hr), on the exocrine pancreas were evaluated in the rat. Single blockage of pancreaticobiliary duct for 4 hr caused a significant rise in serum amylase levels, pancreatic water content, and redistribution of lysosomal enzyme, cathepsin B from the lysosomal fraction to the zymogen fraction, which was considered to mean the colocalization of lysosomal enzymes with pancreatic digestive enzymes in the same subcellular compartment in acinar cells. In addition, the accelerated lysosomal and mitochondrial fragility was observed in the single pancreaticobiliary-duct-obstructed animals. Moreover, the repeated PBDO for 4 hr (2 hr in each obstruction and 1 hr of free flowing of pancreaticobiliary juice between two obstructions) caused more marked changes in almost the all parameters, and the repeated PBDO with intraductal hypertension caused an activation of trypsinogen in the pancreas, making more marked changes in almost the all parameters than the repeated PBDO only group. These results indicate that the present model of repeated PBDO with exocrine stimulation seems to be a pertinent model for gallstone pancreatitis in humans, and that redistribution of lysosomal enzymes and subcellular organellar fragility seem to play an important role in the pathogenesis of pancreatic injuries induced by PBDO, particularly by repeated PBDO with exocrine stimulation, probably via activation of trypsinogen to trypsin by lysosomal enzyme, cathepsin B.
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PMID:A possible mechanism for gallstone pancreatitis: repeated short-term pancreaticobiliary duct obstruction with exocrine stimulation in rats. 767 5

We evaluated the protective effect and the mechanism of action of the trypsin inhibitor, urinastatin, extracted from human urine, in experimental acute pancreatitis induced by a supramaximal dose of cerulein (5 micrograms/kg/hr for 3.5 hr). Urinastatin in a dose of 10,000 units/kg/hr was given by three different methods of continuous infusion: (1) 2 hr before and during cerulein infusion, (2) only during cerulein infusion, and (3) starting 1 hr after the beginning of cerulein infusion and continued for 3.5 hr. In protocol 1 and 2 urinastatin was significantly more protective than in 3. In protocol 1 urinastatin was very protective in all parameters tested (serum amylase level, pancreatic water and amylase content, distribution of lysosomal enzymes, cellular and lysosomal fragility). These results suggest that the administration of urinastatin before and during cerulein infusion may suppress the pathogenesis and evolution of pancreatitis by inhibiting the chain reaction of pancreatic enzyme activation closely related to redistribution of lysosomal enzyme and lysosomal fragility.
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PMID:Effect of urinary trypsin inhibitor on pancreatic cellular and lysosomal fragility in cerulein-induced acute pancreatitis in rats. 768 48

Our previous data showed that the pancreatitis induced in rats by cerulein develops into hemorrhagic pancreatitis following water-immersion stress. The present study examined the effects of water-immersion stress and high doses of cerulein (intraperitoneal injection) on pancreatic blood flow. Five hours of water-immersion stress reduced the local pancreatic blood flow to approximately 30% of the initial value (253.75 +/- 12.58 ml/min/100 g) without causing any histological alterations. Blood flow was decreased as early as 1 h after the immersion and reached the lowest value (30% of initial value) 3 h after the immersion. The administration of 40 micrograms/kg body wt cerulein as two intraperitoneal injections reduced the pancreatic blood flow by 40% 5 h after the first cerulein injection. The injections of cerulein combined with water-immersion stress did not reduce the pancreatic blood flow more than did water-immersion stress alone. The systemic blood pressure was unaffected during 5 h of water immersion after the cerulein injections. These findings suggest that in rats the stress-induced decrease of local pancreatic blood flow may not produce pancreatitis, but may aggravate an existing acute pancreatitis.
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PMID:Role of local pancreatic blood flow in development of hemorrhagic pancreatitis induced by stress in rats. 768 31


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