Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical treatment of gastric and duodenal ulcerations has recently been improved and extended by anti-aggressive and protectively acting drugs (e.g., H2-receptor antagonists and carbenoxolone sodium). However, antacids and anticholinergic treatment are still being used in modern ulcer management. The most important therapeutical measures against chronic relapsing pancreatitis are abstinence from ethanol and surgical treatment of biliary or pancreatic duct obstructions. Symptomatic management--pancreatic enzyme substitution and analgetics, antacids, anticholinergics--is adequate in pancreatic insufficiency and during acute exacerbation, respectively.
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PMID:[Therapy of peptic ulcer and chronic pancreatitis]. 1 65

In acute sodium-taurocholate-induced pancreatitis in the rat, peritoneal dialysis reduced serum amylase levels and the amount of fat necrosis, but did not influence the damage to the pancreas itself. Pancreatic ascites obtained in the early course of the disease was found to have a hypotensive effect when given intraperitoneally to healthy rats. This effect vanished in the later course of acute experimental pancreatitis and was reduced by acidification of the ascites or by administration of an antihistaminic drug. Thus the beneficial effect of continuous peritoneal dialysis on survival time and mortality rate seems to be of systemic origin.
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PMID:Continuous peritoneal dialysis as treatment of acute experimental pancreatitis in the rat. II. Analysis of its beneficial effect. 3 5

The level of adenosine 3':5'-cyclic monophosphate (cAMP) and the activity of adenyl cyclase were studied in the pancreas under normal conditions and during acute hemorrhagic pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. In addition, the adenyl cyclase was localized histochemically in the pancreas. Basal cAMP concentration and adenyl cyclase activity were 0.88 +/- 0.11 pmoles/mg wet tissue and 3.39 +/- 0.21 pmoles/mg protein/min, respectively. The acute pancreatitis drastically reduced the adenyl cyclase activity at 15 minutes to 1.66 +/- 0.54 pmoles/mg protein/min, and totally suppressed adenyl cyclase activity at 30 minutes after the onset of pancreatitis without affecting cAMP levels. The presence of sodium fluoride in the incubation medium prolonged the enzyme activity up to 45 minutes. The progressive disappearance of adenyl cyclase activity presumably resulted from the destruction of cellular integrity caused by autodigestion by the active proteolytic enzymes released during pancreatitis.
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PMID:Adenyl cyclase and cyclic AMP (cAMP) in acute experimental pancreatitis. 18 29

Histological and histochemical study of the pancreas of albino rats and experimental pancreatitis showed the use of sodium thiosulfate to considerably inhibit the progress of necrotic changes and circulatory disturbance. The preparation prevented recidivation of pancreatitis and inhibited sclerotic changes in the gland. Sodium thiosulfate stimulated the regenerative process including regenerative hypertrophy and expressed epimorphosis.
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PMID:[Effect of sodium thiosulfate on the pancreas in experimental pancreatitis]. 36 2

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

The reported complication rate from T-tube infusion of sodium cholate for dissolution of retained biliary stones is low. Among 84 patients reported in the English-language literature, and 10 additional cases of our own, there have been no deaths, an incidence of liver enzyme elevation in 7%, fever in 5%, cholangitis in 2%, and pancreatitis in 2%. Recently, we have infused 100mM sodium cholate at 30 cc/hr into patients through transhepatic biliary stents in an effort to rid the intrahepatic biliary tree of retained stones and biliary sludge. Appropriate precautions were taken to prevent increased biliary pressures by the insetion of a 30 cm manometer into the perfusion system. During four transhepatic infusions in three patients, all experienced nausea and vomiting, and two of the three patients developed diarrhea and abdominal pain. Liver enzymes became elevated during all four infusions, and two of the three patients became septic and died shortly after their infusions. Experimental work in animals suggests that intrahepatic sodium cholate infusion results in injury to the ductal epithelium and predisposes patients to bactermia and sepsis. Even though T-tube infusion of sodium cholate into the common bile duct is well tolerated, direct infusion into the intrahepatic biliary tree through a transhepatic tube is not and carries a high risk of sepsis and death.
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PMID:Sodium cholate dissolution of retained biliary stones: mortality rate following intrahepatic infusion. 43 6

The effect of saline and contrast agents intraductally injected into the pancreatic duct in sufficient volume to cause acinarization was studied in normal rats and in rats with acute pancreatitis. The effect of pancreatic inflammation on the disappearance of injected contrast material was investigated by injecting meglumine diatrizoate and 125I into the pancreatic duct. The activity appeared quickly in the venous blood of normal rats (peak activity at 5 minutes after injection). In rats with sodium taurocholate-induced pancreatitis, the appearance of activity in the blood was retarded. Ninety-two percent of the rats demonstrated pancreatic atrophy or pancreatitis histologically four days following acinarization of intraductally injected saline or metrizamide, meglumine diatrizoate, or meglumine sodium diatrizoate.
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PMID:Contrast absorption and pancreatic inflammation following experimental ERCP. 52 68

Experimental diabetes was produced in 59 rats by intravenous injection of streptozotocin, and the rats were studied from 9 days to 4 months later. Experimental pancreatitis was produced in 28 rats by injecting sodium taurocholate, 3% or 6% solution in saline, into the pancreatic duct. These rats were studied with microangiography from 2 h to 4 days later. Experimental diabetes caused atrophy of the islets of Langerhans but did not cause any changes in the vessels of the exocrine pancreas, liver, or kidney up to 4 months. Capillary filling of the young, long-term diabetic rats was poor in all the examined organs, and the muscle arterioles showed variation of caliber. A 3% sodium taurocholate solution produced mild pancreatitis and little or no changes in the vasculature, whereas a 6% solution caused severe hemorrhagic pancreatitis with local extravasations and poor capillary filling. It is concluded that diagnostically useful vascular changes appear in the pancreas only if severe pancreatitis is present.
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PMID:The effect of experimental pancreatitis and diabetes on the microvasculature of the rat pancreas. 53 1

Sweat electrolytes were carried out in 84 adult patients with calcific pancreatitis, 51 with noncalcific pancreatitis, and the results compared to 37 adult controls. Of the patients with calcific pancreatitis, 33.5% had sweat sodium levels greater than 90 mEq/liter and 14.4% a level greater that 120 mEq/liter. Patients with noncalcific pancreatitis also had a high incidence of elevated sweat sodium levels. Sweat potassium levels were less discriminating, and there appeared to be high sweat calcium levels in a few patients so tested. The reasons for the elevated sweat sodium levels in pancreatitis is not readily apparent, and the possible relationship to heterozygous forms of cystic fibrosis is discussed.
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PMID:Sweat electrolytes in chronic pancreatitis. 62 82

Indomethacin given orally or intramuscularly before or shortly after induction of acute sodium-taurocholate or olive-oil-induced pancreatitis in rats reduced the lethality. Neither the enzyme content of serum, ascites, and pancreatic tissue nor the damage to the organ itself were changed under the influence of indomethacin. Thus a modification of systemic effects of acute pancreatitis may be responsible for the beneficial effect of indomethacin.
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PMID:Indomethacin treatment of acute experimental pancreatitis in the rat. 70 58


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