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

Experimental pancreatitis can be induced by an ethionine-containing, choline-deficient diet in mice. We investigated the role of circulating alpha 1-antitrypsin in this model using two strains of mice: ICR and C57BL-6. A 50% reduction in circulating alpha 1-antitrypsin occurred in all mice by day three of diet exposure. Total protein was reduced by only 9% and albumin was unchanged. Female mice of both strains had significantly lower alpha 1-antitrypsin levels than male mice prior to and after diet exposure. This was associated with significantly greater mortality in both female strains. Interstrain comparisons showed a significantly higher mortality in the C57BL-6 females (100%) compared to the ICR females (58%); this corresponded to significantly lower alpha 1-antitrypsin levels in C57BL-6 females. Regardless of sex or strain, alpha 1-antitrypsin levels prior to and after diet exposure were significantly higher in mice surviving than in mice dying. We conclude that circulating alpha 1-antitrypsin is a predictor of mortality from diet-induced pancreatitis.
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PMID:Alpha 1-antitrypsin levels predict mortality from ethionine-induced pancreatitis in mice. 234 46

The pathogenesis and diagnosis of cirrhotic ascites are reviewed, and the treatment options are described, focusing on pharmacologic management. The major theories on the pathogenesis of cirrhotic ascites are the underfill and overflow theories. The underfill theory states that ascites formation results in decreased plasma volume leading to renal sodium and water retention. The overflow theory states that the initial event in ascites formation is renal sodium retention. Evidence suggests that the formation of ascites is a continuum involving both overflow (early) and underfill (late) mechanisms. Although the most frequent cause of ascites is hepatic cirrhosis, analysis of the ascitic fluid is important to exclude other causes (e.g., neoplasm, peritonitis, pancreatitis). Patients who do not respond to treatment with sodium restriction and bed rest require diuretic therapy. Spironolactone is the agent of choice for treatment of the nonazotemic patient with cirrhotic ascites. Combination therapy with spironolactone and furosemide or spironolactone and metolazone may be used in those patients who do not respond to spironolactone. Patients with impaired renal function should not be treated with spironolactone because of the risk of hyperkalemia. Paracentesis with albumin replacement has been used successfully for treatment of patients with tense cirrhotic ascites. Initial management of cirrhotic ascites is conservative, with sodium restriction and bed rest. Spironolactone is a good first-choice drug for treatment of ascites. Daily weight, serum electrolytes, and renal function should be monitored to assess the effectiveness and potential adverse effects of diuretic therapy.
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PMID:Management of cirrhotic ascites. 267 16

Experimental study had been conducted on 18 healthy adult mongral dogs of both sex, weighting from 7.5-11 kg, randomly divided into four groups. Experimental models of acute hemorrhagic necrotizing pancreatitis (AHNP) were established by retrograde injecting 1 ml/kg of sodium taurocholate directly into the pancreatic duct. The dogs were treated respectively with intravenous infusion of Salviae miltiorrhizae (5 g/kg), 654-2(5 mg/kg) or normal saline. The results showed that PaO2, PaCO2 and pH did not change in early stage of AHNP. The contents of lactic acid dehydrogenase (LDH), albumin and lipid peroxide (LPO) of bronchoalveolar lavage fluid in the AHNP group were significantly higher than that of Salviae miltiorrhizae group (P less than 0.05). The necrosis and disruption of conjunction of endothelial cells resulting from the defects of vascular wall were noted under transmission electron microscope. Both pulmonary vascular and type II pneumocyte were normal in the Salviae miltiorrhizae group. These results suggested that Salviae miltiorrhizae possess the effect of protecting endothelial cells of pulmonary vascular and type II pneumocyte, which could function as scavenger of oxygen-derived free radicals.
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PMID:[Protective effects of Salviae miltiorrhizae and anisodamine (654-2) against early lung injury in acute hemorrhagic necrotizing pancreatitis in the dog]. 273 1

Although parathormone primarily determines normal ionized serum calcium concentration [Ca++] over the long term, it has little impact in the acute situation. Nonhormonal changes in [Ca++] have been related to acute changes in serum pH, but these have been believed small. With use of an experimental model of acute pancreatitis, we measured changes in [Ca++] and related them to changes in other serum constituents known to affect it. All 18 animals studied experienced a decrease in total serum calcium concentration [CaT]. Changes in [CaT] correlated only with changes in protein-bound calcium concentration [CaP] (r = 0.98, p less than or equal to 0.0005). They did not correlate independently with changes in albumin, globulin, or total protein concentration. [CaP] varied as a function of albumin, globulin, and phosphate concentration and pH according to the equation: [CaP] = 17.9 +/- 0.89 [albumin] = 0.68 [globulin] - 2.5 pH + 0.12 [phosphate]. Calculated values for [CaP], when this equation was used, correlated strongly with observed values for [CaP] (r = 0.81, p less than or equal to 0.0005). Measured [Ca++] increased in the animals early during pancreatitis and then returned to baseline levels. A few animals experienced ionized hypocalcemia. [Ca++] correlated only with changes in pH (r = 0.87, p less than or equal to 0.02). The calculated response slope was delta [Ca++]/delta pH = -2.9. It is concluded that pH has a greater effect on [Ca++] than previously recognized. The major determinant of [CaT] during periods of rapid physiologic change appears to be [CaP] while that for [Ca++] is pH.
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PMID:The role of pH in altering serum ionized calcium concentration. 340 67

Regional lung hematocrit ratio (R) was measured in five normal subjects and five patients (2 with pneumonia, 2 with nephrotic syndrome with anemia, and 1 with pancreatitis) using positron emission tomography, a red cell marker 11CO, and a plasma marker [methyl-11C]albumin). The measurements were made in a transaxial thoracic section at midheart level with the subject in supine posture and with a spatial resolution of 1.7 cm. The normal regional hematocrit ratio (means +/- SE) calculated for the lung was 0.90 +/- 0.014, 0.94 +/- 0.023 for the thoracic wall, and 1.00 +/- 0.003 for the heart chambers. The regional lung hematocrit ratio in the patients ranged between 0.81 and 0.86. No correlation was found among the regional lung hematocrit ratio and regional blood volume, lung extravascular density, and the peripheral hematocrit (obtained from venous blood samples). To the extent that 70% of the pulmonary blood in the field of view is in larger vessels with normal hematocrit, the hematocrit in the capillary bed is approximately two-thirds that of the peripheral venous value. Blood volume measurements on the basis of single vascular tracers need to take account of these results.
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PMID:Regional lung hematocrit in humans using positron emission tomography. 348 79

High concentrations of lipid peroxidation (free-radical oxidation) products have been found in bile from patients with recurrent pancreatitis, and the principal component, after hydrolysis, has been identified as an isomerised form of linoleic acid -- typical concentration 25 mmol/l, compared with 4 mmol/l in controls. Chromatographically identical products can be generated by peroxidising linoleic acid using an ultraviolet (UV) source in the presence of albumin, whereas peroxidation by lipoxidase without albumin results in a constellation of products that bear no resemblance to those in biological fluids. These facts, and the suspicion that reflux of abnormal bile may be an initiating mechanism in acute pancreatitis, led us to investigate the effects of linoleic acid peroxidation products in the rat pancreas. Two concentrations of ultraviolet-peroxidised linoleic acid were used (3.6 mmol/l or 25 mmol/l, in a 2.09% solution of bile salts containing albumin 10 g/l) to simulate the human findings and, for comparison, the effects of lipoxidase-peroxidised linoleic acid, 25 mmol/l (in the 2.09% bile salt solution but without albumin), were also studied. 100 microliter of test solution was infused retrogradely into the pancreatic duct using a syringe pump. The results were assessed microscopically at 3-h intervals, and histologically at 12 h: if the animal died before the end of the experiment, the time of death was recorded. Both forms of peroxidised linoleic acid, 25 mmol/l, caused a greater degree of pancreatic injury than that produced by bile salts alone (e.g., macroscopic score at 3 h: ultraviolet, P less than 0.001; lipoxidase, P less than 0.05). Non-peroxidised linoleic acid 25 mmol/l caused less damage than ultraviolet-peroxidised linoleic acid 25 mmol/l, both macroscopically (3 h: P less than 0.01; 12 h: P less than 0.05) and on histology (P less than 0.01). Pancreatic haemorrhage was not a feature.
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PMID:Peroxidised linoleic acid and experimental pancreatitis. 368 Oct 26

Different materials dissolved in 0.9% NaCl were injected into the connective, interlobular tissue of the duodenal part of the rat pancreas. Activated rat pancreatic juice or trypsin were able to induce localized necrohemorrhagic pancreatitis. Only mild edema and leukocytic infiltration were observed after injecting bovine albumin, chinese ink, trypsinogen or nonactivated pancreatic juice. The progression of histological changes was followed for 2 weeks in the trypsin-induced pancreatitis. Limited foci of severe hemorrhage, liquefaction and coagulative necrosis were observed in the first 24 h. Acinar cell degeneration and regeneration were observed 48 h after the operation, fibroblasts appearing in the interlobular spaces. Four days after injection, inter- and intralobular fibrosis, acinar cell degeneration and tubular complexes were observed, presenting a picture characteristic of chronic pancreatitis. Some minimal changes were still seen in the pancreas 1 week after injection, but by the end of the 2nd week the pancreatic histology was normal. These results demonstrate the significance of active trypsin in the pancreatic interstitium with respect to the induction of pancreatitis. This model of localized necrohemorrhagic pancreatitis is highly reproducible and without significant mortality. Following the acute process, histological changes resembling chronic pancreatitis can be observed, but they are completely reversible.
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PMID:Localized necrohemorrhagic pancreatitis in the rat after pancreatic interstitial trypsin injection. Regressive pseudochronic lesions. 373 40

Some patients with hypertriglyceridemia and acute pancreatitis have marked hypocalcemia and high levels of plasma free fatty acids (FFAs). This study tests the hypothesis that increased plasma FFAs can significantly reduce the calcium level in vivo, a phenomenon which is different from local formation of calcium soaps due to lipolysis of adipose tissue lipids. Free fatty acid elevation was induced in rats by the administration of heparin and by the infusion of triglycerides. The results show that, compared with controls, induction of elevated FFA (from 1.57 +/- 0.08 mEq/L to 5.64 +/- 0.35, mean +/- SEM) causes the concentration of calcium to fall rapidly (from 9.04 +/- 0.06 mg/dl to 8.42 +/- 0.10, p less than 0.001). There is a significant (p less than 0.001) positive correlation between spontaneous baseline concentration of FFA and the responsiveness of calcium concentration to FFA challenge. At near-normal levels of FFA there is a significant (p less than 0.001) correlation between the magnitude of increased FFA concentration and decreased calcium concentration. Additional studies in vivo and in vitro show that elevated plasma triglycerides per se did not interfere with measurement of calcium concentration; however, FFA-albumin complexes bind calcium and lower its measured value. These findings suggest that (a) changes in the concentration of FFA occurring spontaneously may affect measured serum calcium concentration; (b) the observed depression of serum calcium concentration may be due in part to intravascular sequestration of calcium by FFA, but increased flux of circulating calcium-FFA complexes into extravascular and intracellular sites may also be important; (c) the markedly increased FFA concentration in some patients with acute pancreatitis may contribute significantly to hypocalcemia and calcium flux in these patients. As parathyroid hormone secretion, function, or integrity may be impaired in pancreatitis, the depressant effect of FFA could be even greater in that disease than in this model.
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PMID:Depression of serum calcium by increased plasma free fatty acids in the rat: a mechanism for hypocalcemia in acute pancreatitis. 402 61

The treatment is described of 17 patients with presumed viral hepatitis who developed hepatic coma unresponsive to standard conservative measures. Five patients were considered for treatment by exchange transfusion. Four were treated, with transient improvement in two, but all died. Nine patients were considered for treatment by heterologous liver perfusion. Six were treated, with transient improvement in two and complete recovery in one. The last patient remains well 12 months later. Dialysis in four patients had no effect on the coma; the addition of albumin to the dialysate did not increase the extraction of bilirubin. The clinical course in most cases was irregular. Complications were common, the most important being cerebral oedema with medullary coning, bleeding, bacterial infection, hypoglycaemia, and pancreatitis. Heterologous liver perfusion was the most efficient method of removing bilirubin. However, it is not yet clear whether it is more effective than exchange transfusion in the treatment of the patient.
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PMID:Management of hepatic coma complicating viral hepatitis. 530 40

The efficacy of steroids, albumin and Trasylol administration in the treatment of experimental pancreatitis was evaluated. An isolated, ex vivo, perfused canine pancreas preparation was used and pancreatitis was initiated by free fatty acid infusion. Steroid administration worsened pancreatitis, Trasylol had no effect, and albumin was markedly effective in ameliorating pancreatitis. These results were interpreted as evidence against enzyme extravasation and for capillary injury as the initial step in the pathogenesis of pancreatitis.
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PMID:Acute pancreatitis. Experimental evaluation of steroid, albumin and trasylol therapy. 615 81


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