Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

In experiments with dogs the influence of controlled respiration with positive endexpiratory pressure (PEEP) on the pancreas was investigated. The pO2 within the tissue was measured during the time of respiration. At PEEP 10 and PEEP 20 an average diminution was observed in the tissue pO2 of 27% and 37%, respectively. A pancreatic edema produced after PEEP 20 was changing into a necrotizing pancreatitis during the following 24 h. At PEEP 10, such a transition was not observed. The pancreatic edema was accompanied by the typical increase in alpha-amylase and lipase activities. After 24 h there were small changes of the enzyme activities in the serum at PEEP 10, whereas at PEEP 20 they were remarkably increased. These results demonstrate that PEEP 20 causes a shortage of oxygen supply of the pancreas. This shortage in connection with an edema can provoke an acute pancreatitis.
...
PMID:[Is there a PEEP-induced pancreatitis in experiments?]. 638 40

In order to investigate whether a relationship exists between in vivo insulin secretion and islet mass, 8 patients suffering from severe chronic relapsing pancreatitis were studied before and after pancreatectomy by glucose-glucagon-test (per os 1.75 g glucose; i.v. glucagon 0.01 mg/kg b.w.) and by intravenous glucose-tolerance-test (iGTT) (i.v. glucose 0.33 g/kg b.w.). Postoperative in vitro assessments of pancreatic insulin and alpha-amylase content were performed, and morphometric studies were carried out. Patients were characterized by reduced c-peptide secretion when compared with healthy subjects. The c-peptide response to the glucose-glucagon-test correlated well with the morphometrically estimated exocrine and islet tissue mass (P less than 0.05) and with the content of insulin and amylase in the tissue. The findings suggest that in subjects suffering from severe chronic relapsing pancreatitis the maximal insulin response might represent a parameter for the patient's islet mass.
...
PMID:Relationship between insulin secretion and pancreas morphology in subjects with chronic pancreatitis. 639 55

The therapeutical efficiency of the new enzyme preparation Triase which contains microbial lipase, protease, and alpha-amylase was studied in dogs with experimental pancreatic failure. Enzyme maldigestion was made by bandaging the great pancreatic duct with pancreatic trypsin injection. The daily therapeutical dose of Triase (4 tablets) eliminated dyspepsia, creatorrhoea, restored body weight. But steatorrhoea was not abolished completely. The fecal fat content decreased to 22.1% versus 33.2% for untreated dogs following 8 weeks of the experiment. The enzyme therapy led to a more rapid reduction in blood amylase and lipase activities. This testifies that pancreatitis ran less severely.
...
PMID:[The therapeutic efficacy of the triase preparation in experimental pancreatic exocrine insufficiency]. 775 59

In experimental models of pancreatitis lipid peroxidation products are increased possibly because of an enhanced generation of oxygen radicals. The purpose of this study was to determine whether lipid peroxidation products are increased in pancreatic tissue and serum of patients suffering from chronic or acute pancreatitis. In 20 patients undergoing operative treatment for chronic (n = 11) and acute pancreatitis (n = 9) the levels of malondialdehyde, conjugated dienes, and reduced and oxidized glutathione were determined in resected tissue samples. The excised tissue was examined and evaluated by light microscopy. Shortly before operation the serum concentrations of malondialdehyde, alpha-amylase, and lipase were measured. Pancreatic tissue from eight organ donors who had no abdominal trauma or pancreatic disease served as control. In chronic pancreatitis, conjugated dienes as well as malondialdehyde concentrations in the tissue were significantly elevated. Reduced glutathione was significantly decreased, suggesting glutathione depletion due to oxidative stress. In acute pancreatitis only the tissue and serum malondialdehyde levels were significantly high, whereas conjugated dienes remained within the normal range. Serum malondialdehyde levels correlated significantly with tissue concentrations (r = 0.76; p < 0.05) but not with the clinical course or the enzyme levels. In chronic pancreatitis, the increased tissue levels of lipid peroxidation products and the changes in glutathione metabolism suggest ongoing peroxidation of lipids due to an enhanced generation of oxygen radicals. In hemorrhagic necrotizing pancreatitis, however, oxygen radical-induced lipid peroxidation cannot be proven. Apparently, other pathomechanisms are involved in the development of the severe tissue damage.
...
PMID:Lipid peroxidation and glutathione metabolism in chronic pancreatitis. 789 58

Ischemia as a causative factor for acute pancreatitis has been discussed for decades but has only recently gained wider acceptance. Chronic pancreatitis, however, has rarely been attributed to ischemic injury. While experimental evidence is available for the ischemic pathogenesis of acute pancreatitis, no studies have been reported about pancreatic ischemia as a single cause of chronic pancreatitis. Also, the progression from acute to chronic pancreatitis has been a very controversial issue. To address both questions we have injected polystyrene microspheres of 20-microns diameter into the pancreatic branches of the splenic artery of 36 rats. Thirteen more rats were sham operated and injected with saline. The animals were killed at 1, 2, 3, and 9 weeks after operation and macroscopically and histologically examined, and serum alpha-amylase and weight gain were determined. For the pancreas the following parameters were assessed using a score from 0 (no change) to 4 (severe change): atrophy, hemorrhage, edema, fat necrosis, acinar necrosis, polymorphonuclear infiltration, mononuclear infiltration, interstitial fibrosis, and ductal changes. While no difference between control and experiment was observed for serum alpha-amylase, weight gain, edema, and hemorrhage, persistent differences were evident for the parameters characteristic of chronic pancreatitis, most significantly for interstitial fibrosis, ductal changes, mononuclear infiltration, acinar necrosis, and atrophy. No spontaneous deaths occurred. The severity of the lesions remained stationary after the first week. Our work shows for the first time that pancreatic ischemia by microvascular hypoperfusion can cause histopathologic changes characteristic of chronic pancreatitis and that these changes follow acute necrotizing pancreatitis.
...
PMID:Does acute pancreatitis progress to chronic pancreatitis? A microvascular pancreatitis model in the rat. 853 54

Two-dimensional gel electrophoresis (2-DE) was used to study protein degradation in human pure pancreatic juice (PPJ) which was collected at 5 min intervals for 20 min by selective endoscopic cannulation of the main pancreatic duct. In PPJ collected from healthy subjects no significant degradation was observed by incubating PPJ at 37 degrees C up to 6 h. By further incubation for 24 h, glycoprotein-1, procarboxypeptidase A-1 and lipase were nearly completely degraded, while alpha-amylase and procarboxypeptidase B-1 were not degraded under these conditions; alpha-amylase became labile in the presence of 1 mM ethylene diaminetetraacetic acid (EDTA) or 10 mM phenyl methyl sulfonyl fluoride (PMSF). Protein degradation was observed by 2-DE of an initial fraction of PPJ collected from patients with chronic calcific pancreatitis (CCP). The 2-DE patterns of subsequent fractions resembled those of PPJ from healthy subjects. The mixture of the last fraction with the initial fraction showed significant protein degradation, inhibited by adding aprotinin. Furthermore, the extent of protein degradation correlated with the dilatation of the main pancreatic duct as a consequence of intraductal stagnation of pancreatic juice. These findings demonstrate that protein degradation in PPJ is accelerated by intraductal activation of serine proteases in the case of patients with CCP. 2-DE of PPJ from patients with CCP provides useful information for the evaluation of intraductal activation of zymogens and the progress of chronic pancreatitis.
...
PMID:Protein degradation in human pure pancreatic juice analyzed by two-dimensional gel electrophoresis. 873 47

Dibutyltin dichloride (DBTC; 6 mg/kg body weight, i.v.) induced acute interstitial pancreatitis in rats. The course of the pancreatitis was examined within 28 days by light and electron microscopy as well as by pathobiochemistry (amylase, lipase, alkaline phosphatase, and bilirubin in serum; tin concentration in biliopancreatic juice, tissue, and concretions). The pathogenesis of the DBTC-induced pancreatitis in rats was studied by different experimental designs (in intact animals, after bile duct ligation, after surgical bypass of the bile duct). DBTC caused toxic necrosis of the biliopancreatic duct epithelium, which is then shed into the duct and forms obstructing plugs in the distal common bile duct. Interstitial pancreatitis occurred during the first 4 days, accompanied by significantly increased activities of serum alpha-amylase and lipase. After 7 days extensive infiltration of the pancreatic interstitium with mononuclear cells was observed. Twenty-eight days after administration of DBTC one-third of the rats showed periductal and interstitial fibrosis as well as an active inflammatory process in the pancreas. The findings suggest a twofold pathogenesis of the DBTC-induced pancreatitis: first, the cytotoxic effects on the biliopancreatic duct epithelium lead to epithelial necrosis with obstruction of the duct, subsequent cholestasis, and interstitial pancreatitis; and second, the hematogenic DBTC effects cause direct injury of pancreatic cells (mitochondrial damage, autophagy, cell necrosis) followed by interstitial edema and inflammation. Both processes lead to this special type of DBTC-induced acute pancreatitis with a tendency to a chronic course, when the obstruction of the duct and cholestasis persist.
...
PMID:Acute interstitial pancreatitis in rats induced by dibutyltin dichloride (DBTC): pathogenesis and natural course of lesions. 936 Oct 94

Difficulties of examining the external secretion of the pancreas by direct secretin-pancreozymin test prompted us to try 4 probe-free methods for functional assessment of the pancreas in 33 patients with chronic acalculous cholecystitis, 50 patients with reactive pancreatitis concomitant with duodenal ulcer, chronic duodenal obstruction, etc., and in 22 patients with primary chronic pancreatitis during a relapse. The Benda-Zheltvai method with assessment of the debit of uric excretion of alpha-amylase during three 30-min intervals before and after standard food loading and calculation of the pancreozymin induction coefficient, assessment of the ratio of alpha-amylase and creatinine clearance from their content in the urine, the proserine provocation urotest, and Lasus test for hyperaminoaciduria resultant from exocrine insufficiency of the pancreas were used. The Benda-Zheltvai method proved to be a sensitive and specific test for the diagnosis of exocrine insufficiency of the pancreas; moreover, it can be used for assessing the treatment efficacy. The proserine test helps assess the type and severity of disorders of pancreatic external secretion. The ratio of alpha-amylase to creatinine clearance demonstrates just the most expressed disorders of pancreatic exocrine secretion during the relapse of primary chronic pancreatitis. Lasus test for hyperaminoaciduria detects pancreatic dyscrinia and provides valuable information about the function of the pancreas.
...
PMID:[Diagnostic evaluation of tubeless methods in the study of external secretions of the pancreas]. 937 19

Oxidative stress has been proposed to play a role in the early events of acute pancreatitis, and metallothionein (MT) can provide protection against oxidative stress. Using transgenic mice, we characterized the effects of depletion of MT-I and -II, or overexpression of MT-I, on pancreatic responses during cerulein-induced acute pancreatitis. In MT-I/-II knockout mice, repeated injections of cerulein caused (a) higher serum amylase levels at 3 and 7 h after the initiation of acute pancreatitis; (b) earlier and stronger upregulation of oxidative stress-responsive genes, including heme oxygenase (HO)-1 and c-fos; and (c) exacerbated tissue damage (edema and polymorphonuclear neutrophil infiltration) compared with nontransgenic 129/SvCPJ mice. Total pancreatic glutathione (GSH + GSSG) content was similar between the knockout and nontransgenic 129/SvCPJ mice. Interestingly, during acute pancreatitis, CD-1 mice pretreated with L-buthionine-[S,R]-sulfoximine (BSO), which dramatically depleted pancreatic GSH, also had more severe pancreatitis, based on the same three criteria listed above, relative to untreated controls. No effects were observed with BSO treatment alone. Finally, during cerulein-induced acute pancreatitis, MT-I overexpressing transgenic mice (>20-fold increase in pancreatic MT-I content) had lower serum alpha-amylase levels between 7 and 24 h and delayed upregulation of HO-1 mRNA levels, but no difference in c-fos mRNA induction relative to the appropriate strain of nontransgenic mice. Diminished tissue damage (particularly cellular necrosis) was noted in these MT-I overexpressing transgenic mice. Total pancreatic GSH content was similar in these transgenic and nontransgenic mice during cerulein-induced acute pancreatitis. These studies suggest that pancreatic MT can function as an intracellular antioxidant as does GSH and that these intracellular antioxidants play a protective role during cerulein-induced acute pancreatitis.
...
PMID:Metallothionein protects against cerulein-induced acute pancreatitis: analysis using transgenic mice. 978 36

The rat pancreas ultrastructure was examined 6, 12, and 18 h after (1) taurocholate-induced acute pancreatitis and after (2) pancreatitis preceded 6 h earlier by intragastric acute 40% ethanol ingestion (5 g/kg b.w.). Pancreatic specific trypsin activity and plasma alpha-amylase were assayed at the same time intervals. The antecedent acute ethanol ingestion resulted in the evident aggravation of pancreas ultrastructural alterations. Acute pancreatitis preceded by ethanol resulted in the increase of zymogen granules number, RER channels were more irregularly distributed, autophagosomes were more abundant and degeneration of mitochondria was more advanced when compared to acute pancreatitis without ethanol ingestion. Tryptic activity increased to higher degree in all pancreatitis groups preceded by ethanol, but this difference was statistically significant (P < 0.01) only after 18 h. These morphological (but not biochemical) differences progressed 12 h after pancreatitis induction. After 18 h of acute pancreatitis the number of zymogen granules decreased in previously alcoholized rats, but tryptic activity remained twofold higher that in animals not given ethanol. Other signs of cellular impairment were still more prominent in alcoholized rats. The obtained results suggest that even single acute ethanol abuse prior to acute pancreatitis does aggravate the morphological and biochemical lesions observed in this disease with possible negative consequences for the prognosis.
...
PMID:The effect of antecedent acute ethanol ingestion on the pancreas ultrastructure in taurocholate pancreatitis in rats. 982 48


<< Previous 1 2 3 4 5 Next >>

---