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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complexity of pathogenesis and clinical observations of acute pancreatitis demands a simultaneous experimental investigation at various structural and functional levels. The induction of acute pancreatitis by transformation of a pancreatic edema after short-term pancreatic ischemia was used for studies on the contribution of an alteration of energy metabolism to pathogenesis. The experiments demonstrate that in 70 percent of the rats the pancreatic edema was transformed into acute pancreatitis by 20 min ischemia. This was checked by morphological and enzymic means. For studying the influence of short-term ischemia in the cellular metabolism of acinar cells, pancreatic exocrine cells have been isolated from normal pancreas or that altered by ischemia. These cells were morphologically characterized and their capacity of energy metabolism was quantified.
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PMID:A hierarchic approach for experimental investigations into the pathogenesis of acute pancreatitis. 240 44

Acute pancreatitis was initiated in the isolated ex vivo, perfused canine pancreas preparation by exposing the gland to a 2 hour period of ischemia before a 4 hour perfusion period. The pancreatitis was manifested by edema formation, weight gain, and hyperamylasemia. When the osmotically active agent albumin was added to the perfusate at the end of the ischemic period, virtually no edema developed, weight gain was minimal, and the amylase level remained within normal limits during the subsequent 4 hour perfusion period. This suggests that a change in capillary permeability may be an early step in the pathogenesis of ischemia-induced pancreatitis in this experimental model.
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PMID:Experimental ischemic pancreatitis: treatment with albumin. 241 56

Transcatheter arterial embolization (TAE) has been widely used for treatment of hepatocellular carcinoma. Acute pancreatitis occasionally occurs as a complication of TAE. We have investigated the possible effects of TAE on the pancreas by monitoring serum pancreatic enzyme activities following TAE with various embolic materials. Serum amylase activity was increased very little in the patients treated with chemotherapy alone or plus TAE with lipiodol, slightly increased in many of the patients treated with chemotherapy plus TAE with gelatin sponge, and increased in all of the patients treated with chemotherapy plus TAE with gelfoam powder. The activity was increased to a level as high as 700 U/dl or more in most individuals of the last category. In one of them acute pancreatitis developed, probably because the gelfoam powder regurgitated into the pancreaticoduodenal artery, and occluded a very peripheral portion of the pancreatic vascular bed, leading to ischemia of the pancreas. These results suggest that choosing the correct particle size is important for prevention of acute pancreatitis.
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PMID:Acute pancreatitis after transcatheter arterial embolization (TAE) for hepatocellular carcinoma. 247 61

A 65 year old woman, who had a giant umbilical hernia since more than 30 years, was admitted for a transitory cerebrovascular ischemia. During her stay, she presented an episode of acute pancreatitis localized in the head of the pancreas. All current causes of acute pancreatitis were ruled out, especially alcoholism and gallstones. Endoscopic retrograde cholangio-pancreatography performed in the patient lying on the left side demonstrated localization of the antrum and the duodenum with the head of the pancreas into the umbilical hernia. It seems clear that the giant umbilical hernia caused a progressive and intermittent passage of the head of the pancreas through chronic traction on the ligament of Treitz and acute pancreatitis by incarceration. At our knowledge, this mechanical cause of acute pancreatitis was not yet described in the literature.
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PMID:[Acute pancreatitis caused by a voluminous umbilical hernia. Case report]. 248 14

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

To study the importance of a disturbed energy metabolism for the development of acute pancreatitis (AP) rats pretreated either by induction of a juice edema or by intraductal trypsin instillation were subjected to temporary pancreatic ischemia. By means of a scoring system quality and quantity of pathomorphologic parameters were quantified 24 h postoperatively. There was a clear correlation between macroscopic and histologic scores independent of the model used. While a juice edema or 40 min ischemia alone did not induce AP, a combination of both led in half of the animals treated to AP. This was mainly characterized by extrapancreatic fat necrosis. Besides less specific fat necrosis the histologic examination of the pancreas revealed acinar necroses at the periphery of the lobules as a frequent injury pattern. After trypsin injection a persistent pancreatic edema, hemorrhages, fat and parenchymal necroses were typical findings. Both focal centro-lobular and extended sublobular or lobular necroses were histologically observed. An additional temporary ischemia augmented significantly the severity of findings, however, their quality was not essentially changed. From the present results it can be concluded that an alteration of the pancreatic energy metabolism, e.g. by hypoperfusion or ischemia, may be an important pathogenic factor in precipitating experimental AP.
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PMID:Effect of temporary ischemia upon development and histological patterns of acute pancreatitis in the rat. 274 64

The influence of long-term (26 weeks) and long-term plus acute ethanol administration on the development of acute pancreatitis was studied in rats. While both these treatments alone did not induce pancreatitis in any rat, extrapancreatic fat necrosis and histologic lesions of the pancreas were found in the majority of animal 24 hours after additional establishing of a pancreatic juice edema by an obstruction/hypersecretion mechanism. Severity and frequency of findings were significantly increased by additional short-term ischemia (25 min) of the pancreas. In control rats without ethanol ingestion, the edema receded without any lesions, and after additional ischemia significantly fewer rats exhibited signs of acute pancreatitis when compared to the ethanol-treated groups. An experimental model of acute alcoholic pancreatitis is presented with ethanol ingestion, temporary ductal obstruction and stimulation of secretion being essential constituents, which may be of clinical relevance, too.
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PMID:Experimental acute pancreatitis in rats after chronic and chronic plus acute ethanol administration in combination with a pancreatic juice edema. 275 27

To study the dynamics of pathomorphologic alterations in the development of acute pancreatitis (AP) and the corresponding changes of the patterns of pancreatic enzymes in rats AP was induced by: 1) combination of a pancreatic juice edema and temporary pancreatic ischemia, ii) by intraductal instillation of trypsin, and iii) by trypsin instillation in combination with ischemia. At 4, 8 and 24 h postoperatively the histologic findings and the activities of lipase and alpha-amylase in the pancreas and the serum were analyzed. The histologic sum score of the individual rats did not correlate with their enzymic patterns in pancreas and in serum. In all three models there was a development of parenchymal necrosis independent of the existence of pancreatic fat necrosis. Therefore, it is not probable that fat necrosis represents an obligatory precondition for the initiation of autodigestion.
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PMID:Experimental acute pancreatitis--a quantification of dynamics at enzymic and histomorphologic levels. 281 89

The biochemical characterization of experimental acute pancreatitis was performed by determination of the secretory enzymes lipase and alpha-amylase, of the cytoplasmic ALAT (alanine aminotransferase), of total protein and calcium concentration in serum of rats. The moderate and protracted course of the pathological process in the small animal model presented allowed to study the initial phase from 1-24 h. In the first 4-8 h most massive enzyme release into the intravasal space was observed. The level of enzyme activities was correlating with the severity of assault. One noxa alone (ischemia or juice edema) resulted in a moderate enzyme release (lipase : 2-2.5 fold of control). The action of both noxae caused a drastical increase in enzyme activities in the initial phase lipase : 8-20 fold, ALAT: 7 fold, alpha-Amylase: 2.5 fold). 24 h postoperatively the serum enzyme activities were at distinct pathological level. At this time acute pancreatitis provoked already a decreased serum protein content. A hypocalcemia was not observed.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. II. Behaviour of serum parameters. 349 93


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