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

With a view toward the therapeutic use of somatostatin in the treatment of acute pancreatitis, a preliminary investigation was conducted with 6 healthy volunteers, in which the suppressive effect of somatostatin on endocrine and exocrine pancreatic function was observed. A 30-minute baseline measurement period was followed by the administration of cyclic somatostatin (100 microgram by i.v. injection plus a 90-minute infusion at a rate of 200 microgram/hr). After the first 45 minutes of this infusion secretion was submaximally stimulated by the infusion of secretin-cholecystokinin-pancreozymin (CCK-PZ) (75 U each), over two hours. No decrease was observed in basal bicarbonate or enzyme concentration under somatostatin administration alone. However, secretion did not show the usual steep rise after the commencement of stimulation. After the somatostatin infusion was stopped, i.e. under secretin-CCK-PZ alone, a significant increase occurred in the values of secretin-induced volume, bicarbonate concentration and total bicarbonate contents of the duodenal aspirate, as well as in CCK-PZ-induced enzyme secretion. The release of insulin, both basal and stimulated, was also significantly decreased by somatostatin.
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PMID:[Suppressive effect of somatostatin on secretin-CCK-PZ-stimulated endocrine and exocrine pancreatic function in man (author's transl)]. 41 Jan 66

Alpha amylase of pancreatic origin is cleared by the kidney more rapidly than the salivary isoamylase. To determine whether alterations in the ratio of pancreatic to salivary amylase in sera caused alterations in over all renal clearance, the clearance of amylase was measured before and after the exocrine pancreas was stimulated with a prolonged intravenous infusion of secretin plus cholecystokinin. Serum and urine samples collected prior to and following stimulation were analyzed for amylase activity and creatinine concentration. Amylase isoenzymes were separated using isoelectric focusing. Over all renal clearance of amylase and of the separated amylase isoenzymes were calculated as a percentage of the clearance of creatinine. The hormone infusion was associated with an increase in serum and urine amylase activities, this increase being mainly accounted for by pancreatic amylase. The renal clearance of the salivary and pancreatic isoamylases was not altered by the hormone infusion but the over all amylase clearance by the kidney rose from 2.31 +/- 0.74 to 3.42 +/- 1.46% of creatinine clearance. In some cases the renal clearance of amylase following stimulation entered the range considered diagnostic for acute pancreatitis.
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PMID:Effect of pancreatic stimulation on serum and urine amylase isoenzymes in man. 51 99

The inhibitory action of both calcitonin (CT) and glucagon (GK) on human pancreatic secretion has been evaluated in detail. The reduction of enzyme secretion expressed as percentage corresponded to 60--80% of the initial values in response to both CT and GK when the hormones were given as single infusions during background stimulation with secretin or with secretin plus cholecystokinin-pancreozymin (CCK-PZ). After withdrawal of GK-infusion the return to normal values of enzyme secretion was distinctly faster than after CT, thus reflecting a more rapid degradation of circulating GK than of CT. In the presence of stimulation with secretin plus CCK-PZ, the combined administration of CT and GK did not enhance the inhibitory actions of CT and GK. Fluid and bicarbonate secretions were not affected by either CT or GK. The results suggest that CT and GK inhibit human pancreatic enzyme secretion by similar modes of action. Therefore, the combined administration of both CT and GK does not offer a reasonable approach to the treatment of acute pancreatitis.
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PMID:Similar modes of action of calcitonin and glucagon in inhibiting pancreatic enzyme secretion in man. 54

Exocrine pancreatic function after secretin and cholecystokinin stimulation was examined in a group of patients with idiopathic necrosis of the femoral head and in a normal control group. The volume output, bicarbonate and amylase concentrations in the patient group were not significantly lower than in the control group. Taken individually, however, 3 out of 8 patients with idiopathic necrosis of the femoral head had abnormal pancreatic function tests. In 4 patients there was a significant alcohol intake, with a history suggestive of acute pancreatitis in 2. This suggests that in some patients chronic pancreatitis may be a factor in the pathogenesis of idiopathic necrosis of the femoral head.
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PMID:Exocrine pancreatic function in patients with idiopathic necrosis of the femoral head. 73 63

To evaluate the action of somatostatin on exocrine and endocrine pancreatic function, synthetic somatostatin (GIF) was administered (intravenous bolus of 300 mug followed by a constant 60-minute infusion, 5 mug/min) to 17 normal subjects. The secretin-induced volume and total bicarbonate contents of the duodenal aspirate were not affected whereas the bicarbonate concentration was significantly diminished. GIF reduced decisively the pancreatic enzyme secretion stimulated by pure (99%) cholecystokinin-pancreozymin. After the GIF infusion was stopped, a significant rise in enzyme secretion was observed. The secretin-induced insulin release was almost completely suppressed. Because GIF can be extracted in large quantities from pancreas, these data suggest that somatostatin may play a physiological role in the regulation of the secretory processes of this organ. Furthermore, GIF may be a useful adjunct in the treatment of acute pancreatitis.
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PMID:Effects of somatostatin on exocrine and endocrine pancreatic function stimulated by intestinal hormones in man. 76 55

The effect of an elemental diet on canine exocrine pancreatic secretion was evaluated by infusing an elemental diet into the duodenum of dogs and monitoring the output of the pancreas. The stimulatory properties of the elemental diet were compared with a nearly equimolar dose of an L-form neutral amino acid, 0.16 normal hydrochloric acid, and 2 units per kilogram per hour of exogenous cholecystokinin. Intraduodenal infusion of elemental diet produced significant increases in pancreatic volume and protein output. These changes were similar to those produced by the amino acid solution and suggest that the stimulatory properties of the elemental diet are primarily due to the amino acid content. The results of the this study suggest that elemental diets stimulate the duodental mucosa to secrete cholecystokinin which stimulates the exocrine pancreas. Elemental diets administered in such a manner that the substance passes through the duodenum would not theoretically be a satisfactory method of providing calories to patients with acute pancreatitis.
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PMID:The effect of an intraduodenal elemental diet on pancreatic secretion. 112 75

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

A brief report is given on the possible role of oxygen-derived free radicals and cholecystokinin in the pathogenesis of experimentally induced acute pancreatitis. Furthermore, use of scavengers (superoxide dismutase, catalase), CCK-receptor antagonists and somatostatin are discussed in the therapy of acute pancreatitis induced in animal models. It is suggested that both the term of direct pancreatic cytoprotection of the above-mentioned agents and the validity of the animal models used for induction of acute pancreatitis have to be reconsidered.
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PMID:Pancreatic cytoprotection: new approaches. 134 8

Studies in animal models suggest that oxygen radicals may be important in the pathogenesis of acute pancreatitis. Because glutathione is an essential component of the defense against radical-mediated cellular injury, we investigated whether pancreatic glutathione content is influenced by inducing acute pancreatitis and whether augmenting the intracellular supply of glutathione would alter the course of pancreatitis. Caerulein, a decapeptide cholecystokinin analogue, induces acute necrotizing pancreatitis in mice when given in high doses (50 micrograms/kg per h) over a period of 6 h. The pancreatic glutathione content (total, GSH + GSSG) in mice treated with high-dose caerulein fell to 17% of normal within 4 h of beginning caerulein and recovered toward normal after discontinuing caerulein treatment. Mice treated with glutathione monoethyl ester (20 mmol/kg 1 h before caerulein, 10 mmol/kg 3 and 7 h after starting caerulein) were found to have blunted depletion of pancreatic glutathione, diminished histologic evidence of pancreatitis (necrosis, inflammation, and vacuolization), and lower serum amylase values compared with mice treated with caerulein alone. These findings suggest that the profound depletion of pancreatic glutathione caused by hyperstimulation of the pancreas with caerulein is critically important in the pathogenesis of acute caerulein-induced pancreatitis.
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PMID:Glutathione monoethyl ester ameliorates caerulein-induced pancreatitis in the mouse. 137 Feb 92

The role of exogenous and endogenous cholecystokinin has been studied in the process of pancreatic regeneration after acute pancreatitis. A mild form of pancreatitis was induced in rats by subcutaneous cerulein at 12 micrograms.kg-1, three times a day for 2 days. After 3 days of rest, the cerulein-treated rats were divided into four groups: rats with acute pancreatitis fed 20% casein, who received no treatment; rats fed 50% casein; rats fed 20% casein supplemented with 1% soybean trypsin inhibitor (SBTI); and rats fed 20% casein who received 1 microgram.kg-1 of subcutaneous cerulein, three times a day. Controls were fed 20% casein plus saline subcutaneously. Rats were killed after 5, 10, or 20 days of treatment. Pancreatitis resulted in significant decreases in pancreatic weight and contents of protein, amylase, chymotrypsin, RNA and DNA. During the regenerative process, 1 microgram.kg-1 of cerulein increased all parameters to control values within 5 days and induced pancreatic growth thereafter. SBTI restored the pancreas to normal after 10 days with cellular hypertrophy; the 50% casein diet gave a response similar to SBTI without hypertrophy. It can be concluded that cerulein and SBTI can accelerate pancreatic regeneration after an attack of acute pancreatitis.
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PMID:Soybean trypsin inhibitor and cerulein accelerate recovery of cerulein-induced pancreatitis in rats. 137 Jun 63


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