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

Oxyhemoglobin dissociation curves were performed from blood of subjects with pancreatitis associated with Type V and Type I hyperlipoproteinemia. The hemoglobin-oxygen affininty was markedly increased with P50 varying from 22.3 to 17.7 mmHg. As the hyperlipoproteinemia subsided the clinical and laboratory signs of pancreatic affection disappeared. The increased hemoglobin-oxygen affinity and decreased flow of red cells due to hyperchylomicronemia in the microcirculation may lead to tissue hypoxia, which may act as a precipitating injurious factor leading to pancreatitis during severe hyperlipemia.
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PMID:Increased hemoglobin-oxygen affinity in patients with pancreatitis associated with type I and V hyperlipoproteinemia. 2 74

Studies of coagulation were performed prospectively in 41 patients with mild to moderately severe acute pancreatitis. Six patients (15%) presented with coagulation data suggestive of defibrination; two of them had clinical signs of bleeding. No other cause than pancreatitis was found in these 6 patients to account for coagulation abnormalities. Comparing the patients who presented defibrination to those who did not, no difference was observed in clinical course and admission values of serum amylase, fibrinogen, urea, calcium, glucose, transaminase levels, white blood cell count and arterial partial pressure of oxygen. Platelets counts and serum creatinine levels were respectively lower and higher in the first group of patients.
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PMID:[Defibrination syndrome during acute pancreatitis: 6 cases. Prospective studies of coagulation in 41 patients (author's transl)]. 46 Nov 54

A canine model was devised to measure the oxygen consumption of the pancreas in experimentally induced pancreatitis. Over the 120 minute investigation period the oxygen consumption fell by 63% in the presence of a diminishing pancreatic blood flow and constant arteriovenous percentage saturation across the pancreas. Dextran 40 has been previously shown to maintain the pancreatic circulation. Accordingly a second group of dogs was treated with Dextran 40 (1.5 ml/kg) 60 minutes after induction of the pancreatitis. This produced a significant increase in the pancreatic oxygen consumption and widening of the arteriovenous difference. Dextran 40 appears to reverse the hypoxia of the pancreas noted in acute experimental pancreatitis.
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PMID:Experimental acute pancreatitis: the changes in pancreatic oxygen consumption and the effect of Dextran 40. 51 73

Three hundred patients with acute pancreatitis have been studied. Pancreatitis was associated with alcoholism in 207, biliary tract disease in 51 and other conditions in 42. Twenty-two patients died, and an additional 34 patients required more than one week of treatment in the intensive care unit. Retrospective analysis of the first 100 patients identified 11 objective findings which correlated with the occurrence of serious illness or death. They were, on admission, age over 55 years, blood glucose level over 200 milligrams per cent, white blood count over 16,000 per cubic millimeter, serum lactic dehydrogenase level over 350 International units per liter and serum glutamic-oxalacetic transaminase level over 250 Sigma Frankel units per cent. During the initial 48 hours of therapy, the findings were hematocrit value decrease over 10 percentage points, serum calcium level below 8 milligrams per cent, base deficit over 4 milli-equivalents per liter, a blood urea nitrogen level increase over 5 milligrams per cent, estimated fluid sequestration over 6 liters and arterial oxygen tension less than 60 millimeters of mercury. Prospective application of these signs in the latter 200 patients permitted the accurate early identification of those with severe pancreatitis. Only one of 162 patients with fewer than three of these early features was seriously ill or died, while 24 of 38 patients with three or more early positive findings were seriously ill or died. The objective early identification of patients with severe pancreatitis permits more vigorous management of this group and also provides a basis for the selection of patients for the evaluation of proposed improved therapies. Percutaneous peritoneal dialysis in severe pancreatitis was evaluated in ten patients, with three or more positive early signs, who were randomly assigned to dialysis or continued conventional care. Morbidity was strikingly reduced in patients who underwent dialysis, and while death or more than nine days of intensive care occurred in two of five patients who did not receive dialysis, all five patients having dialysis recovered after fewer than nine days of intensive care treatment. Serious illness or death occurred in 31 of the first 100 patients but in only 26 of the more recent 200 patients. There has been a similar fall in mortality from 15.0 to 3.5 per cent. Factors which may contribute to this improvment include the objective early identification of patients with severe disease, the avoidance of early laparotomy whenever practical, the prolongation of nasogastric suction until all evidence of pancreatic inflammation has resolved, careful monitoring of respiratory function and early treatment of pulmonary complications and peritoneal dialysis in patients with severe disease.
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PMID:Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. 94 Oct 75

Twenty-nine patients, divided into three groups: 1) chronic obstructive pulmonary disease; 2) acute or chronic pulmonary disease with left heart failure; 3) respiratory insufficiency after peritonitis, pancreatitis, and/or sepsis, were studied during respirator treatment with regard to gas exchange, breathing mechanics and central circulation. The dead space ventilation was somewhat greater in group 1 than in the other groups. The alveolar-arterial oxygen tension difference was least in group 1, greater in group 2 and extremely high in group 3. Neither dynamic compliance of the thorax nor inspiratory resistance showed any significant differences between the groups. The cardiac output had the highest values in group 3. The venous admixture was generally small in group 1 and extremely large in group 3. The pulmonary artery pressures were highest in group 2. Three variables proved to be valuable when assessing the prognosis of a patient: a large venous admixture; a large alveolar-arterial oxygen tension difference, and a high pulmonary artery pressure indicated a less favourable prognosis.
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PMID:Studies on pulmonary function in patients during respiratory treatment. Diagnostic and prognostic evaluations. 99 53

A supramaximal dose of caerulein (5 micrograms/kg.hr for 3.5 hours) caused an acute pancreatitis with marked hyperamylasemia and intense interstitial edema in rats. In this model of pancreatitis, the redistribution of lysosomal enzyme in acinar cells as well as the increased lysosomal and mitochondrial fragility were also observed. The combined therapy of a low molecular weight protease inhibitor, FOY, a synthetic platelet activating factor (PAF) antagonist, CV 6209, and a xanthine oxidase inhibitor, allopurinol produced more significant improvements in all the parameters examined than the therapy of any only one of these three agents, each only one therapy exerting a partial significant protective effect. These results indicate that several factors, such as unknown proteases activities, PAF and oxygen-derived free radicals may be involved in the pathogenesis of pancreatic injuries in this caerulein-induced pancreatitis. These results also suggest that such a combined therapy of different kinds of agents, whose therapeutic mechanisms are also different, is useful in the clinical treatment of acute pancreatitis.
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PMID:"Cocktail" therapy for acute pancreatitis: combined therapy of protease inhibitor, xanthine oxidase inhibitor and platelet activating factor antagonist in rat caerulein-induced pancreatis. 130 81

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

To define the role of free radicals and of lipid peroxide involvement during the progress of cerulein-induced acute pancreatitis in mice, we evaluated the effect of a novel free radical scavenger, 2-octadecylascorbic acid (CV-3611), on pancreatic edema formation, and the levels of serum enzymes (amylase, lipase) and of lipid peroxide in pancreatic tissue. Mice were divided into three groups: control group, intraperitoneal injection of saline only; pancreatitis group, cerulein 50 micrograms/kg injected intraperitoneally six times at 1-hr intervals; treatment groups, CV-3611 10 mg/kg subcutaneously just after intraperitoneal cerulein injection. After the cerulein injection, the degree of pancreatic edema formation, serum amylase and lipase levels, and the amount of lipid peroxide in pancreatic tissue increased significantly during the observation period of 12 hr. Treatment with CV-3611 resulted in significant reduction in pancreatic edema formation at 3.5 hr (P less than 0.05) and 9 hr (P less than 0.05), serum amylase and lipase levels at 3.5 hr (P less than 0.05) and 12 hr (P less than 0.05), and lipid peroxide levels at 3.5 hr (P less than 0.05), 6 hr (P less than 0.05) and 12 hr (P less than 0.05). These results indicate that a novel free radical scavenger, CV-3611, has a strong therapeutic effect during the development of acute pancreatitis and suggest that oxygen-derived free radicals play an important role in the pathogenesis of acute pancreatitis.
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PMID:Evidence for a role of free radicals by synthesized scavenger, 2-octadecylascorbic acid, in cerulein-induced mouse acute pancreatitis. 137 Sep 33

Oxygen-derived free radicals mediate an important step in the initiation of experimental acute pancreatitis. Thereby these reactive oxygen metabolites are generated at an early stage of disease. The source of the enhanced production of oxygen radicals remains unclear. Experimentally, the efficiency of scavenger treatment varied between different models, whereby these differences were depending on the experimental model and not on the form of pancreatitis which was induced. Most studies pretreated the experimental animals before inducing acute pancreatitis. This does not mirror the clinical reality, since patients are admitted to the hospital after onset of the disease. It was shown in Cerulein-pancreatitis, however, that scavenger treatment also mitigated the pancreatic tissue damages after induction of acute pancreatitis. Moreover, antioxidant treatment also attenuated the extrapancreatic complications, thus improving the final outcome of the disease. The first indirect observations also suggest that in human acute recurrent and chronic pancreatitis oxygen free radicals are generated and add to the damages seen. Therefore, well-defined controlled clinical studies with patients suffering from acute pancreatitis are needed to validate the role of oxygen radicals in this disease.
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PMID:[Oxygen radicals and acute pancreatitis]. 147 89

There is a growing body of experimental and clinical evidence to suggest that oral or rectal administration of 5-ASA or 5-ASA conjugates is associated with significant adverse side effects including pancreatitis, hepatitis, and renal toxicity. The objective of this study was to assess the ability of 5-ASA to interact with low-molecular-weight iron to yield oxygen-derived free radicals and to determine whether these oxidants could damage model biological compounds. We found that 5-ASA was very effective at chelating ferric iron (Fe3+), and it rapidly reduced Fe3+ to the ferrous form (Fe2+). Addition of the 5-ASA/Fe2+ chelate to solutions containing polyunsaturated fatty acids or deoxyribose resulted in lipid peroxidation and oxidative carbohydrate degradation, respectively. These results are consistent with the formation of the highly reactive (and cytotoxic) hydroxyl radical. Formation of this free radical species was confirmed by the ability of hydroxyl radical scavengers (dimethyl sulfoxide, dimethyl thiourea) to inhibit the 5-ASA/Fe-mediated oxidative reactions. Maximum hydroxyl radical formation was achieved at a 5-ASA-to-Fe3+ ratio of 1.0 (20 microM 5-ASA and 20 microM Fe3+). Increasing this ratio significantly inhibited OH. formation with a concomitant reduction in lipid peroxidation and deoxyribose degradation. Finally, we demonstrated that 5-ASA promotes the reductive release of Fe3+ from ferritin. Data obtained in this study suggest that 5-ASA may, under certain conditions, promote the formation of potentially injurious free radical species. These oxidative reactions may contribute to some of the adverse side effects known to be associated with the newer preparations of 5-ASA.
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PMID:Prooxidant properties of 5-aminosalicylic acid. Possible mechanism for its adverse side effects. 150 90


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