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

This study describes the effect on the function and structure of the saline-perfused cat pancreas of factors implicated in the pathogenesis of pancreatitis (bile acid, ethanol, pancreatic enzymes) after their addition to the perfusion fluid or their instillation into the pancreatic duct. Instillation of trypsin or chenodeoxycholic acid, but not ethanol, into the pancreatic duct resulted in a profound suppression of secretory function. The leakage of perfusion fluid and amylase from the gland was also abruptly increased. Intraarterial perfusion of trypsin also inhibited secretin-induced flow and cholecystokinin evoked enzyme secretion. Intraarterial bile acid inhibited fluid flow but augmented enzyme secretion in a concentration-dependent manner. In addition, massive or focal parenchymal necrosis was caused by sustained intraarterial perfusion of bile acid or trypsin, respectively. Elastase and phospholipase A had little influence on pancreatic function or structure when added to the perfusion fluid. These findings show that pancreatic structure and function can be disturbed by potentially toxic factors administered not only via the ductal system but also via the vascular route, and consequently suggest that an "internal reflux" mechanism could be involved in the pathogenesis of pancreatitis in addition to a "ductal reflux" mechanism.
Pancreas 1988
PMID:Analysis in the isolated perfused cat pancreas of factors implicated in the pathogenesis of pancreatitis. 245 94

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.
Pancreas 1988
PMID:Parenteral superoxide dismutase plus catalase diminishes pancreatic edema in sodium taurocholate-induced pancreatitis in the rat. 246 Aug 55

We have recently reported successful 72-h preservation of the canine pancreas with a new cold-storage solution developed at the University of Wisconsin (UW solution). Over 10 mo, we performed 11 combined pancreas-kidney and 4 isolated-pancreas transplants with this solution. In situ cooling of the donor pancreas was performed with 1000 ml of UW solution followed by ex vivo perfusion with an additional 250-500 ml. Graft preservation times ranged from 3 to 19 h (mean 10.2 h). Pancreas transplants were vascularized whole-organ grafts with pancreaticoduodenocystostomy. Early graft function was excellent as assessed by immediate insulin independence, high urinary amylase and low serum amylase levels, and a technetium perfusion index indicating good pancreatic blood flow. There were no episodes of primary nonfunction, graft pancreatitis, or vascular thrombosis. Actuarial patient and graft survival at 1 mo was 92.9%. We conclude that UW solution provides excellent early graft function for up to 19 h of cold storage. Based on previously reported data on its efficacy in liver and kidney preservation, UW solution seems ideally suited as a universal intra-aortic flush and cold-storage solution.
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PMID:Use of UW solution in pancreas transplantation. 246

Acute edematous pancreatitis was produced in rats by subcutaneous administration of caerulein. Pancreas weight, pancreas histology and plasma amylase were used as endpoints to quantitate the severity of the syndrome. A caerulein dose of 10 micrograms/kg.hour produced the most severe pancreatitis, whereas at 5 micrograms/kg.hour the values were half-maximal. The pancreatic lesions were characterized by edema, formation of cytoplasmic vacuoles, leukocytic infiltration, necrosis, and with time (12-hour caerulein infusion) dilated acini. Cholecystokinin octapeptide also produced pancreatitis when given at ten times the dose required for caerulein (50 micrograms/kg.hour instead of 5 micrograms/kg.hour). Carbachol did not induce pancreatitis. Two prostaglandins, 16,16-dimethyl prostaglandin E2 injected subcutaneously and prostaglandin E2 infused subcutaneously, dose dependently prevented caerulein-induced pancreatitis (pancreatic edema, leukocytic infiltration, and necrosis) and reduced the number and size of intracellular vacuoles. The ED50 were 15 to 25 micrograms/kg for 16,16-dimethyl prostaglandin E2 and 90 micrograms/kg.hour for prostaglandin E2. Neither prostaglandin, given at doses inhibiting the development of pancreatitis, prevented the retardation of gastric emptying caused by caerulein, a finding suggesting that the prostaglandins may act specifically on the effect of caerulein on the pancreas but not on caerulein receptors in gastric smooth muscle. Indomethacin, an inhibitor of prostaglandin synthesis, and methscopolamine bromide, an anticholinergic agent, had no effect on caerulein-induced pancreatitis. We concluded that prostaglandins of the E type prevent the development of caerulein-induced pancreatitis. The mechanism by which prostaglandins protect the pancreas may involve stabilization of lysosomes within the acinar cells and inhibition of intracellular activation of pancreatic digestive enzymes.
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PMID:Prevention by prostaglandins of caerulein-induced pancreatitis in rats. 246 59

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.
Pancreas 1989
PMID:Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning. 247 70

The effects of cholecystokinin receptor antagonist CR 1392 was studied in a model of mild acute pancreatitis induced in rats by four subcutaneous injections of the secretagogue caerulein. A single subcutaneous injection of 50 mg/kg body weight of CR 1392 caused a dramatic reduction in serum amylase concentration and pancreatic wet weight as well as histologic improvement of the caerulein-induced acute pancreatitis when given 30 min before the first caerulein injection. CR 1392 was also effective in reducing the elevated serum amylase activity, pancreatic weight, and histologic alterations even when administered after the pancreatitis had been induced. These present observations suggest that CR 1392 remains active for more than 3 h and blocks the action of caerulein on the pancreas.
Pancreas 1989
PMID:Effect of a new cholecystokinin receptor antagonist CR 1392 on caerulein-induced acute pancreatitis in rats. 247 65

The activation of zymogen proteases and lysosomal enzyme cathepsin B in the pancreas was investigated in cerulein-induced pancreatitis in rats. Acute pancreatitis was induced by two intraperitoneal injections of 40 micrograms/kg of body weight of cerulein at intervals of 1 h. After the first cerulein injection, the active trypsin and elastase contents in the pancreas tissues significantly increased, and reached the highest level at 3 h after the first injection, followed by peaks at 5 h in the serum amylase and lipase levels and the pancreas wet weight. Cathepsin B contents in pancreas tissues showed a parallel increase with active zymogen enzymes during the first 3 h of pancreatitis. These findings may suggest that the intracellular activation of trypsinogen is an important step in the development of cerulein-induced acute pancreatitis and that cathepsin B plays a role in the activation of trypsinogen in pancreatic acinar cells.
Pancreas 1989
PMID:Activation of proteases in cerulein-induced pancreatitis. 247 99

This study was performed to assess the effects of misoprostol (M), a synthetic prostaglandin E1 analog, on experimental pancreatitis in rat. Pancreatitis was induced by ligation of the main pancreatic duct of 3-month-old male Wistar rats. Pancreatic lesions were observed at 6, 12, 24, 48, and 96 h after pancreatic duct ligation (PDL). A time of 48 h was chosen to evaluate M treatment. M was injected intraperitoneally (500 micrograms/kg every 4 h) between time 0 and 48 h after PDL. Stereological analysis was performed on light and electron microscopy. Total pancreatic amylase and chymotrypsin concentrations were determined. Four groups of five rats were studied: sham operated (SO), M without PDL (PG), duct ligation without M (DL), and duct ligation with M (DLPG). Edema, dedifferentiation of pancreatic acinar cells, and heterogeneous distribution of zymogen granule diameters observed after PDL were significantly decreased by M in the DLPG group. Enzyme concentrations were also decreased by M in the DLPG group. Enzyme concentrations were also decreased by M both in normal (PG) and duct ligated rats (DL). M has protective effects against pancreatic lesions induced by PDL. In this model, the protective effect of M may be due to a blockade of the autodigestive secretions of the pancreatic acinar cells.
Pancreas 1989
PMID:Protective effect of misoprostol, a synthetic prostaglandin E1 analog, on experimental pancreatitis induced by pancreatic duct ligation in rat. 247 2

To quantitate pancreatic stone protein (PSP), a competitive radioimmunoassay using monoclonal antibodies to PSP extracted from pancreatic stones and a sandwich enzyme-linked immunosorbent assay (ELISA) using monospecific polyclonal antibodies to the secretory forms of PSP (PSP S) were established. When PSP concentrations were measured in pancreatic juice by radioimmunoassay, no difference could be found between patients suffering from chronic calcifying pancreatitis and other diagnostic groups. Yet, with the ELISA technique involving polyclonal antibodies, decreased concentrations were found in chronic calcifying pancreatitis patients when compared to controls (p less than 0.001), chronic alcoholics without pancreatic symptoms, or obstructive pancreatitis patients. These discrepancies are discussed. The monoclonal antibodies recognizing the C-terminal part of PSS S (PSP S1), results from the radioimmunoassay indicate that the concentration of that polypeptide is identical in the juice of controls and patients. Results from the ELISA obtained with polyclonal antibodies raised against PSP S2-5 molecules, i.e., recognizing the PSP S1 part and the N-terminal portion of the molecule, indicate that the differences observed reflect differences in the juice concentration of that N-terminal peptide.
Pancreas 1989
PMID:Pancreatic stone protein: quantification in pancreatic juice by enzyme-linked immunosorbent assay and comparison with other methods. 251 Jan 47

Experimental pancreatitis can be induced by an ethionine-containing, choline-deficient diet in mice. We investigated the role of circulating alpha 1-antitrypsin in this model using two strains of mice: ICR and C57BL-6. A 50% reduction in circulating alpha 1-antitrypsin occurred in all mice by day three of diet exposure. Total protein was reduced by only 9% and albumin was unchanged. Female mice of both strains had significantly lower alpha 1-antitrypsin levels than male mice prior to and after diet exposure. This was associated with significantly greater mortality in both female strains. Interstrain comparisons showed a significantly higher mortality in the C57BL-6 females (100%) compared to the ICR females (58%); this corresponded to significantly lower alpha 1-antitrypsin levels in C57BL-6 females. Regardless of sex or strain, alpha 1-antitrypsin levels prior to and after diet exposure were significantly higher in mice surviving than in mice dying. We conclude that circulating alpha 1-antitrypsin is a predictor of mortality from diet-induced pancreatitis.
Pancreas 1989
PMID:Alpha 1-antitrypsin levels predict mortality from ethionine-induced pancreatitis in mice. 234 46


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