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

The effects of pancreatic intraductal infusions of the surface active pancreatic ductogram enhancing agent, polyoxyethylene hydrogenated castor oil, were studied in the dog. Moderately high pressure retrograde infusions of 5 per cent polyoxyethylene hydrogenated castor oil into the main pancreatic duct resulted in pancreatitis-like changes significantly greater than those seen in the saline solution control group. These changes persisted despite buffering of the agent to physiologic pH and the elimination of nonphysiologically high pressure by direct ductal perfusion. Similar inflammatory changes were associated with ductal perfusion using oleic and, to a lesser degree, ricinoleic-fatty acids at concentrations of 10(-4) molar sufficient to account for the titratable acidity of 5 per cent polyoxyethylene hydrogenated castor oil. It is postulated that residual-free fatty acids may play some role in polyoxyethylene hydrogenated castor oil related toxicity. The surface active properties of the agent may also be involved. Caution and further research are recommended prior to widespread use of the agent in endoscopic retrograde pancreatography.
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PMID:Experimental pancreatitis after surfactant exposure. 617 35

This study was initiated to clarify whether the main hydrolytic enzymes of the pancreas are activated or inactivated when secreted into the stomach of patients who had undergone a pylorus-preserving pancreaticoduodenectomy (PPPD) and were given a pancreaticogastrostomy (PG) for the reconstruction. Seventeen such patients, 15 cancer patients and two pancreatic patients, who underwent PPPD-PG reconstruction were postoperatively followed up for 3 or more years to investigate the influence of the gastric acid on the p-type amylase and lipase activity. Results revealed that when the pH was < 3.0, both the p-type amylase and the lipase secretion remained inactivated, but when the pH was > 3.1, the activity of both enzymes increased proportionately. The pancreatic enzyme activity in the small intestine was also investigated in seven patients, six cancer cases and one case of pancreatitis, given a PPPD-PG reconstruction, and it was found that the pancreatic enzyme activity in the small intestine increased after milk loading. Further, the fecal pancreatic enzyme activity was investigated in 17 patients given a PPPD-PG reconstruction. Results reveal that the fecal p-type amylase, lipase, and chymotrypsin activity amounted to 21, 27, and 31% of the respective values seen in 10 healthy volunteers. However, the fecal pancreatic enzyme activity levels did not differ significantly from the levels seen in 20 pancreaticoduodenectomy patients given a pancreaticojejunostomy reconstruction. In conclusion, it was found that the main hydrolytic enzymes of the pancreas are activated when the gastric acidity is over pH 3.1, which normally occurs after ingestion of a meal.
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PMID:Pancreatic enzyme activity after a pylorus-preserving pancreaticoduodenectomy reconstructed with pancreaticogastrostomy. 857 82

The chief dangers reported with some common drugs are reviewed. Hazards of antibiotic therapy include: the increasing incidence of sensitization to penicillin with occasional anaphylactic reactions; aplastic anemia with chloramphenicol, and the poor tolerance of infants for chloramphenicol; staphylococcal enterocolitis; unnecessary "prophylactic" use of antibiotics. Thiazide diuretics may precipitate potassium depletion, skin reactions, pancreatitis, blood dyscrasias, gout, diabetes mellitus and hepatic coma. Reserpine can increase gastric acidity, induce mental depression, and when used with digitalis lead to ventricular premature beats. Hydralazine may aggravate angina pectoris, cause tachycardia, and bring about a syndrome resembling disseminated lupus erythematosus. Guanethidine may result in loose stools, impotence, and postural hypotension. Hazards of phenothiazines include jaundice, parkinsonian states and tremors, convulsions, hypotension, and blood dyscrasias. The butanediols have numerous side effects including gastrointestinal, cutaneous and hypotensive reactions. Prolonged corticosteroid therapy introduces a new danger in surgical treatment. The progesterone-like drugs may induce masculinization of the female fetus.
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PMID:Dangers in the use of some potent drugs. 1398 37

Cell-death programs executed in the pancreas under pathological conditions remain largely undetermined, although the severity of experimental pancreatitis has been found to depend on the ratio of apoptosis to necrosis. We have defined mechanisms by which apoptosis is induced in pancreatic acinar cells by the oxidant stressor menadione. Real-time monitoring of initiator caspase activity showed that caspase-9 (66% of cells) and caspase-8 (15% of cells) were activated within 30 min of menadione administration, but no activation of caspase-2, -10, or -12 was detected. Interestingly, when caspase-9 activation was inhibited, activation of caspase-8 was increased. Half-maximum activation (t(0.5)) of caspase-9 occurred within approximately 2 min and was identified at or in close proximity to mitochondria, whereas t(0.5) for caspase-8 occurred within approximately 26 min of menadione application and was distributed homogeneously throughout cells. Caspase-9 but not caspase-8 activation was blocked completely by the calcium chelator BAPTA or bongkrekic acid, an inhibitor of the mitochondrial permeability transition pore. In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione. We conclude that the oxidative stressor menadione induces two independent apoptotic pathways within pancreatic acinar cells: the classical mitochondrial calcium-dependent pathway that is initiated rapidly in the majority of cells, and a slower, caspase-8-mediated pathway that depends on the lysosomal activities of cathepsins and is used when the caspase-9 pathway is disabled.
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PMID:Caspase-8-mediated apoptosis induced by oxidative stress is independent of the intrinsic pathway and dependent on cathepsins. 1743 Dec 16

The mechanism described for maintaining the optimum level of gastric acidity is designated by Boldyreff as the "self regulation of the acidity of the contents of the stomach." In support of Boldyreff's hypothesis is the evidence obtained from many experiments carried out both on man and on animals, in which solutions of alkali and acid have been placed in the stomach. The introduction of acid fluid has led to a regurgitation of alkaline duodenal contents, whereas the introduction of alkaline solutions has called forth a secretion of acid gastric juice. The experiments reported in this paper were carried out for the purpose of ascertaining how the stomach would react, in as far as the secretion of hydrochloric acid is concerned, to a more or less continuous influx of relatively strong alkaline fluid, prolonged throughout the cycle of digestion. Numerous studies have shown that any serious interference with the process of regurgitation leads to a rise in the acidity level of the stomach; i.e., to a state of hyperacidity. There is but little evidence, however, to indicate whether the acidity level will be depressed temporarily or permanently (hypoacidity) when alkaline material, in considerable amounts, continues to enter the stomach. The influx of alkaline fluid was provided for by transplanting the larger pancreatic duct into the wall of the stomach after ligating and dividing the lesser duct. Specimens of test meal for analysis were withdrawn through gastric fistulas made after the method of Janeway. Animals prepared in this manner served also to furnish additional information regarding the possible relation of the hydrochloric acid of the gastric juice to certain acute inflammatory and chronic sclerotic changes in the pancreas. From the results of these experiments it appears that the presence of a considerable amount of pancreatic juice in the stomach throughout the period of digestion leads only to a moderate decrease in the acidity level of the ingesta in the later stages of digestion. Earlier in the process there is no constant alteration of the acidity level in either direction. The findings then serve not only to corroborate the views of Boldyreff, but also to demonstrate the remarkable compensatory activity of the gastric glands under conditions which entail an unusual quantity of alkali in the stomach. In addition the work has shown that when the larger pancreatic duct is properly transplanted into the wall of the stomach, it may remain patent for months. In animals in which this operative procedure has been carried out, the pancreas has been found to undergo no inflammatory or other degenerative changes. This finding is regarded as evidence against the postulation of Hlava that gastric juice is probably responsible for the occurrence of certain cases of acute hemorrhagic pancreatitis.
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PMID:THE DIVERSION OF THE PANCREATIC JUICE FROM THE DUODENUM INTO THE STOMACH. ITS EFFECTS UPON THE LEVEL OF GASTRIC ACIDITY AND UPON THE PANCREAS. 1986 86

The gastrointestinal (GI) mucosal barrier is continuously exposed to noxious toxins, reactive oxygen species, microbes, and drugs, leading to the development of inflammatory, erosive, and ultimately ulcerative lesions. This report offers a consensus opinion on the rational administration of GI protectants to dogs and cats, with an emphasis on proton pump inhibitors (PPIs), histamine type-2 receptor antagonists (H2 RAs), misoprostol, and sucralfate. These medications decrease gastric acidity or promote mucosal protective mechanisms, transforming the management of dyspepsia, peptic ulceration, and gastroesophageal reflux disease. In contrast to guidelines that have been established in people for the optimal treatment of gastroduodenal ulcers and gastroesophageal reflux disease, effective clinical dosages of antisecretory drugs have not been well established in the dog and cat to date. Similar to the situation in human medicine, practice of inappropriate prescription of acid suppressants is also commonplace in veterinary medicine. This report challenges the dogma and clinical practice of administering GI protectants for the routine management of gastritis, pancreatitis, hepatic disease, and renal disease in dogs and cats lacking additional risk factors for ulceration or concerns for GI bleeding. Judicious use of acid suppressants is warranted considering recent studies that have documented adverse effects of long-term supplementation of PPIs in people and animals.
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PMID:ACVIM consensus statement: Support for rational administration of gastrointestinal protectants to dogs and cats. 3037 11