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

A variety of radiographically demonstrable colon abnormalities associated with pancreatitis are illustrated. Extensive changes of either localized or diffuse inflammation are more common than has generally been appreciated. Localized changes may mimic carcinoma. Transverse colon inflammation secondary to pancreatitis may be appreciated on plain abdominal radiographs and to better advantage with a contrast enema. This pattern is distinctive and suggests a severe underlying pancreatitis. A water soluble contrast enema is recommended if there is any evidence of colon necrosis or fistula. Recognition of all of the changes of pancreatitis may lead to earlier management of the severe complications.
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PMID:Inflammation and necrosis of the transverse colon secondary to pancreatitis. 41 59

Jejunal perfusion studies were performed to assess water, electrolyte, d-xylose, and d-glucose transport in 16 patients with chronic calcific pancreatitis (eight with and eight without steatorrhoea) and in 10 control subjects. The patients with steatorrhoea demonstrated significantly less xylose, water, and electrolyte absorption than patients without steatorrhoea and control subjects, when an isosmotic slaine-xylose solution was perfused. On the other hand, when an isosmotic saline-glucose solution was perfused, the patients with steatorrhoea absorbed significantly more glucose, water, and electrolytes than control subjects. Significant correlation was demonstrated between the absorption of xylose as measured by the segmental perfusion technique and the peak serum xylose level during perfusion as well as the five-hour urinary xylose excretion after a 25 g oral dose of xylose. The xylose absorption measured by small bowel perfusion also correlated significantly with pancreatic juice amylase and trypsin concentrations obtained during a standard pancreatic function test.
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PMID:Jejunal monosaccharide, water, and electrolyte transport in patients with chronic pancreatitis. 62 5

Rat were given 2.5 mg/kg/day prednisolone in drinking water during 1.5 to 12.5 months and an equal group of matched controls received only water. A pathological study of the pancreas and a physiological study of exocrine pancreatic secretion have been done. The most significant pathological effects at 1.5-12.5 months of steroids are dilatation of acini, flattening of duct epithelium, and the presence of protein plugs in the ducts. The most significant functional modifications at 9-11 months of treatment are increased concentrations and output of proteins both in basal and stimulated pancreatic secretion of steroid-treated rats. This is very similar to the results observed by our group in alcohol-induced pancreatitis. It is assumed that the hyperconcentration could be at least partly responsible for precipitation of proteins and the precipitate formation for the lesions. For the large group of acute or chronic pancreatic lesions characterized by the formation of protein plugs in the ducts, the term catarrhal pancreatitis is proposed.
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PMID:Secretory pattern and pathological study of the pancreas of steroid-treated rats. 67 93

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

We have developed a canine model which allows simultaneous quantification of pancreatic enzyme outputs, duodenal volume flow, and pancreatic and duodenal pressures under physiological circumstances. Twelve studies on 4 conscious healthy dogs demonstrated that mean fasting pancreatic pressure was 5 to 10 cm H2O higher than mean fasting duodenal pressure. Furthermore, 8 min after ingestion of a meal, both the pancreatic and the duodenal pressure increased. Surprisingly, the mean duodenal pressure was higher than the mean pancreatic pressure 20 min after feeding. This relationship lasted for 30 min. Lastly, elevation of postprandial pancreatic pressure occurred concomitantly with increased pancreatic enzyme output, and duodenal pressure increased with increased duodenal volume flow. The observed large postprandial duodenal volume flows associated with duodenal pressures greater than pancreatic duct pressures may favor reflux of duodenal contents into the pancreatic duct. These relationships may be important in the pathogenesis of postprandial pancreatitis and in the induction of pancreatic cancer.
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PMID:Relationships between fasting and postprandial pancreaticoduodenal pressures, pancreatic secretion, and duodenal volume flow in the dog. 90 81

To investigate the mechanism by which the pancreatic acinar cells are injured in animals with an obstructed common channel, we measured the amount of lysosomal enzymes and of amylase in the pancreatico-biliary juice in rats with pancreatico-biliary duct obstruction (PBDO). We tested the protective effect of a new potent synthetic protease inhibitor, E3123 (4-guanidinobenzoate methanesulfonate), on the exocrine pancreas in this model of PBDO and secretin infusion. Blockage of PBD for 4 hours and secretin (0.2 CU/kg.hr) infusion caused a significant rise in portal serum amylase and cathepsin B levels, pancreatic water content, and pancreatic amylase content, as well as redistribution of cathepsin B in acinar cells. These changes tended to continue for 12 hours after the removal of PBDO and disappeared at 24 hours. All the changes induced by PBDO with secretin infusion were no longer observed at 48 hours. The administration of 5 mg/kg.hr of E3123 during PBDO markedly attenuated all the parameters examined in this study. Thus, it had a significant protective effect on acinar cells in this model. E3123 in a dose of 2 mg/kg.hr had a partial, but significant, protective effect. These results indicate the possible usefulness of E3123 in the treatment of pancreatic duct obstructed pancreatitis.
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PMID:Effect of short-termed pancreatico-biliary duct obstruction on lysosomal enzyme in rats: protective effect of a potent new protease inhibitor, E-3123. 128 76

This study was designed to evaluate the effects of direct pancreatic surface cooling on the exocrine pancreas. We measured the changes in serum amylase levels, pancreatic water, amylase and cathepsin B as a lysosomal enzyme, content, histological changes of acinar cells, and the subcellular distribution of cathepsin B after 1-2- and 3-hours of direct pancreatic cooling in rats. In addition, we evaluated the in-vivo amylase and cathepsin B output stimulated by caerulein, in-vitro lysosomal and mitochondrial fragility as well as the pancreatic adenylate energy metabolism. 2-hours cooling showed slight yet significant changes, but 3-hours cooling caused most significant changes including hyperamylasemia, increased pancreatic amylase content and very mild histological changes. Furthermore, 3-hours cooling caused a remarkable redistribution of cathepsin B activity from the lysosomal fraction to the heavier zymogen fraction, and colocalization of the lysosomal enzyme with the digestive enzyme, the impaired amylase and cathepsin B output into pancreatic juice stimulated by caerulein as well as the accelerated fragility of lysosomes and mitochondria, and impaired pancreatic adenylate energy metabolism. These results indicate the impaired exocrine pancreatic functions induced by direct pancreatic cooling injury induced by cooling as shown in the other models of experimental pancreatitis. Moreover, this cooling model of pancreatitis seems to be useful in understanding the early events in the pathogenesis of acute pancreatitis, and we must take these "cold" injuries of exocrine pancreas into considerations, particularly in the pancreas transplantation and in other major abdominal surgeries where the pancreas is exposed to cooling.
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PMID:Effect of hypothermia on pancreatic acinar cells in rats. 128 73

A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the level of metabolic "stress" on acinar cells, have been shown to mitigate the severity of acute pancreatitis in a number of models. Not all studies have shown a benefit, however, and differences may exist between different structural classes of antagonists. Because increased pancreatic stimulation due to loss of feedback inhibition of CCK has been proposed to contribute to the pain of some patients with chronic pancreatitis, CCK receptor antagonists could also be of benefit in this setting. Somatostatin and its analogs diminish pancreatic secretion of water and electrolytes and have been effective in treating pancreatic fistulas and pseudocysts. These agents are also being evaluated for their ability to reduce pain in chronic pancreatitis (perhaps by reducing ductal pressure by diminishing secretory volume) and mitigating the severity of acute pancreatitis (possibly by reducing the metabolic load on acinar cells). Recently described secretin receptor antagonists may also have therapeutic value as a means of selectively inhibiting pancreatic secretion of water and electrolytes.
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PMID:Receptor strategies in pancreatitis. 134 60

To determine whether a synthetic somatostatin analogue, octreotide, and a cholecystokinin receptor antagonist, L-364,718, may be beneficial in acute pancreatitis, 33 dogs were assigned to four groups. Each dog underwent laparotomy with injection of autologous bile into the dorsal pancreatic duct. Thirty minutes after the induction of pancreatitis, Group 1 received a subcutaneous injection of octreotide (200 micrograms/kg), Group 2 received an equal volume of the octreotide carrier, Group 3 received an hourly intravenous bolus of L-364,718 (60 micrograms/kg), and Group 4 received an equal volume of the L-364,718 carrier. Hemodynamic profiles, arterial blood gases, plasma glucose, and serum amylase were obtained before laparotomy, at bile injection, and at hourly intervals. The pancreas was removed after 8 hours for gross evaluation, measurement of water content, and histologic examination. A significant decrease in cardiac index and a significant increase in serum amylase and pancreatic edema occurred in all four groups 8 hours after the induction of pancreatitis (P less than 0.05), but there was no statistical difference between any group. Likewise, there was no difference in gross or histologic changes in the pancreas of any group. The somatostatin analogue, octreotide, and the cholecystokinin receptor antagonist, L-364,718, did not ameliorate the effects of severe, bile-induced pancreatitis in dogs.
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PMID:Effect of somatostatin analogue and cholecystokinin receptor antagonist on bile-induced acute canine pancreatitis. 137 11

Phase I clinical trials of the purine analog 2',3'-dideoxyinosine (ddl) revealed that 10% of the patients developed pancreatitis, yet there was no clear relationship between increasing doses of ddl and the development of pancreatitis. To test the effects of chronic ddl administration on the structure and function of the rat pancreas, male Wistar rats were given ddl at 100 mg/kg/day i.p. for 35 days or 1400 mg/kg/day for 30 days, in two divided doses. Serum amylase levels, pancreatic tissue water content (edema) and pancreatic morphology by light and electron microscopic examination of pancreata from ddl-treated rats were similar to those of rats receiving saline injections only (controls). 2',3'-Dideoxyinosine administration did not alter the subcellular distribution of the lysosomal enzyme cathepsin B, whose redistribution to a more dense zymogen granule-enriched subcellular fraction is an early indicator of acute pancreatitis. Dispersed pancreatic acini from rats receiving ddl (100 mg/kg/day for 30 days) were incubated in vitro for 15 min with either caerulein or carbamylcholine as secretory stimuli. There was no detectable difference in the stimulatable amylase secretion from ddl-treated animals compared to the control group. Based on these findings, we conclude that ddl has no direct toxic effect on the rat pancreas. 2',3'-Dideoxyinosine may be contributing to pancreatitis in acquired immunodeficiency syndrome patients by potentiating other pancreatotoxic agents or by its action on a pancreas that is already altered by the human immunodeficiency virus infection.
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PMID:In vivo and in vitro effects of the azidothymidine analog dideoxyinosine on the exocrine pancreas of the rat. 137 99


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