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

Scavengers of toxic oxygen reduction products have been reported to reduce the inflammatory reaction in some models of pancreatitis. In a blinded study, the effect of parenteral pretreatment with superoxide dismutase plus catalase was compared with placebo on pancreatitis induced in rats by infusion of 0.25% or 2% sodium taurocholate into the hepatopancreatic duct. The degree of inflammation was assessed by macroscopic examination of the pancreas, dry/wet weight ratios of pancreatic specimens, amylase activity in plasma and peritoneal exudate, the weight of the exudate, and its content of total protein. All parameters were indicative of a more severe inflammation in rats given the higher concentration of sodium taurocholate. The only significant effect of the superoxide dismutase plus catalase treatment was a moderate reduction of the dry/wet weight ratio, i.e., pancreatic edema, in rats given 2% sodium taurocholate. Our results indicate that toxic oxygen reduction products, available for interception by parenterally administered superoxide dismutase plus catalase, are of only minor importance in the pathogenesis of sodium taurocholate-induced pancreatitis in the rat.
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PMID:Parenteral superoxide dismutase plus catalase diminishes pancreatic edema in sodium taurocholate-induced pancreatitis in the rat. 246 Aug 55

The effect of a synthetic protease inhibitor, gabexate mesilate (GM), which was administered directly into the pancreatic duct, on acute pancreatitis induced by sodium taurocholate in dogs was investigated. Intraductal administration of GM significantly inhibited intrapancreatic trypsin activity at 24 h, compared with the control. The survival rate 10 days after initiation of pancreatitis for the group in which GM was administered intraductally was 100%, whereas that for the control group was 25%. Serial blood biochemical analysis and histopathological findings suggested that the progress of pancreatitis was favorably influenced by intraductal administration of GM.
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PMID:Prevention of the spread of experimental acute pancreatitis by intraductal administration of a synthetic protease inhibitor in dogs. 246 86

The effect of blood exchange transfusion on experimental acute pancreatitis was investigated. Acute hemorrhagic pancreatitis was induced in rats by the injection of sodium taurocholate into the pancreatic duct. One hour after the induction of pancreatitis, blood exchange transfusion was carried out in these rats. The survival rates by 24 hr significantly increased in the exchange transfusion group as compared to those in the non-treated control group. Blood exchange transfusion, though had not significant effect on the macroscopic findings at autopsy, reduced pulmonary edema. These results suggested that blood purification by exchange transfusion may be beneficial for patients with acute pancreatitis, especially at an early stage.
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PMID:Effect of blood exchange transfusion as an initial treatment of acute hemorrhagic pancreatitis. 246 34

1. Survival time, amylase activity and pancreatic protein, DNA and RNA content were measured in 38 control rats and in 104 rats injected with sodium taurocholate to induce acute pancreatitis after 21 days on one of four diets differing in protein, lipid and carbohydrate content. 2. All of the parameters measured were lower in rats with pancreatitis than in controls maintained on the same diets. Among the rats with pancreatitis, those receiving a protein-free diet survived longer and had significantly higher DNA, lower amylase activity and lower RNA and protein levels than those receiving a balanced diet or one that was high in protein or lipid content. 3. We conclude that acute pancreatitis in rats has a more benign course in protein-undernourished animals.
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PMID:Protective effect of a protein-free diet in acute experimental pancreatitis. 248 Jan 66

The damage to the liver during acute pancreatitis (AP) could be partly dependent on depressive action of pancreatitis associated ascitic fluid (PAAF) on the energy metabolism of hepatocytes. The aim of the study was to assess the effect of PAAF from dogs with acute experimental pancreatitis (AEP) and from humans with AP on the respiratory function of isolated rat liver mitochondria (RLM). The mitochondrial oxygen consumption rate in state 3 respiration (with ADP) and in state 4 (without ADP) using sodium succinate as substrate and oxygen Clark's electrode was estimated. Respiratory control ratio (RCR) and P/O ratio were calculated. PAAF was collected after 6 h of AEP induced by Elliott's method in 8 dogs, and from 4 patients with AP, intraoperatively. Both animal and human PAAFs increase the oxygen consumption rate by RLM in state 4 dose dependently (by 65% with 50 microL to 150% with 200 microL of canine PAAF). This uncoupling effect of human PAAF was twice more potent than the canine. Dialysis of PAAF reduced this effect almost completely. The mitochondrial ATPase activity in RLM treated with PAAF was stimulated and this effect was also reduced by dialysis. The conclusion was that the damage to the liver in AEP could be partly dependent on the toxicity of dializable component(s) of PAAF on the energy metabolism of mitochondria. These findings may partly explain the beneficial effects of peritoneal lavage in acute pancreatitis.
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PMID:The effect of pancreatitis associated ascitic fluid on some functions of rat liver mitochondria. A possible mechanism of the damage to the liver in acute pancreatitis. 248 Sep 84

The ability of atrial natriuretic peptide (ANP) to preserve renal function in dogs with hypovolemic acute renal insufficiency was tested in anesthetized dogs 4 h after the induction of acute pancreatitis. Plasma volume had decreased by 21.5% and glomerular filtration rate (GFR) by 43.2%. Blood pressure had declined by 30 mmHg. ANP was given intravenously at 50 and 150 ng.kg-1.min-1. With the lower dose, blood pressure (BP), GFR, and clearance of p-aminohippuric acid (CPAH) did not change but urine flow (V) and sodium excretion (UNaV) increased. With the higher dose, BP declined by 25 mmHg, GFR declined, but V and UNaV still increased. When plasma volume was maintained with 4% colloid during the progression of pancreatitis and ANP 50 ng.kg-1.min-1 given, BP declined, GFR did not change, and there was a magnified increment in V and UNaV. The administration of glucagon (5 micrograms/min iv) to dogs with hypovolemic pancreatitis caused BP to decline by 17 mmHg. Despite a major increment in GFR, fractional excretion of sodium increased only slightly, compared with that obtained with ANP. We conclude that glucagon preserves GFR more effectively than ANP in hypovolemia, but ANP is more effective in protecting urinary water and sodium excretion.
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PMID:Response to atrial natriuretic peptide in dogs with hypovolemic acute pancreatitis. 252 75

The pancreatic release of arachidonic acid metabolites was studied in a porcine model of acute pancreatitis. In situ isolation of the pancreatic gland enabled selective collection of pancreatic venous blood, pancreatic lymph, and ascites fluid. Three experimental groups were studied: 1) control (n = 9); 2) hemorrhagic pancreatitis induced by injection of 5% bile salt (sodium taurocholate) into the pancreatic duct (n = 10); and 3) edematous pancreatitis induced by injection of free fatty acid (FFA) into the pancreatic artery (n = 10). Determinations of cyclooxygenase metabolites were performed by radioimmunoassay; lipoxygenase metabolites (LTC4, LTD4) were measured by radioimmunoassay after purification by high-performance liquid chromatography. Prostaglandin (PG)F1 alpha, thromboxane B2, and PGF2 alpha concentrations were almost doubled in the lymph of the FFA group during pancreatitis, as were PGF1 alpha levels in pancreatic venous blood. However, concentrations of cyclooxygenase metabolites remained unchanged in the control group and in the bile salt group. Concentrations of LTC4 and LTD4 in lymph and ascites fluid of both pancreatitis groups increased from about 50 pg/ml to a mean level of 600 pg/ml at 6 h. Leukotriene concentrations in the control group were consistently below 50 pg/ml. The results of this study indicate that above all LTC4 and LTD4 are released from the organ and that these arachidonic acid metabolites may be also involved in the events following acute pancreatitis contributing to the systemic effects of the disease.
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PMID:Release of arachidonic acid metabolites during acute pancreatitis in pigs. 260 7

A model of acute necroto-hemorrhagic pancreatitis was prepared by injecting 5% sodium taurocholate-trypsin solution directly into the pancreatic duct of the rat. Fourty eight hours before the preparation of acute pancreatitis, intraductal injection of 0.1%, 0.2% or 0.4% sodium taurocholate-trypsin solution as mild irritant was able to decrease the mortality to 27%, 17% and 17% respectively. The maximal elevation of the serum amylase concentration in acute pancreatitis was decreased to 43%, 47% and 54%, respectively. Microscopic examination of the pancreatic tissue of the rats which were alive after pretreatment of mild irritants showed that the acute pancreatitis was milder and there was a tendency to change to chronic pancreatitis. Thus, we conclude that there is a phenomenon of adaptive cytoprotection on the exocrine pancreas in rats. The mechanisms of the phenomenon remain to be explored.
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PMID:[The adaptive cytoprotection of exocrine pancreas in rats]. 260 56

Two technical modifications have been suggested for whole-pancreas transplantation with bladder drainage. The duodenal button technique (DB [Madison]) and the duodenal segment technique (DS [Iowa]) are the most commonly performed procedures (1,2). From December 1985 until May 1988 we performed 32 combined pancreas-kidney transplants using DB and DS techniques in 17 and 15 patients, respectively. Bladder leaks, pancreatitis, bleeding episodes, and surgically related infections were all decreased with the duodenal segment technique. Metabolic acidosis was more common with DS but was easily managed with oral sodium bicarbonate. The one-year actuarial graft survival with DB is less when compared with DS (76.1% vs. 87.5%). Three technical graft losses occurred with DB vs. none with DS. One graft was lost in each group to rejection. Our results indicate that the duodenal segment technique of bladder implantation adds safety to whole-pancreas transplantation and must now be considered the procedure of choice.
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PMID:Comparison between duodenal button and duodenal segment in pancreas transplantation. 264 20

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


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