Acute Necrotizing Pancreatitis
Mostrando 13-22 de 22 artigos, teses e dissertações.
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13. Glutathione monoethyl ester ameliorates caerulein-induced pancreatitis in the mouse.
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 su
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14. Behavior of antibiotics during human necrotizing pancreatitis.
The aim of the study was to verify whether antibiotics excreted by the normal pancreas are also excreted in human necrotizing pancreatitis, reaching the tissue sites of the infection. Twelve patients suffering from acute necrotizing pancreatitis were treated with imipenem-cilastatin (0.5 g), mezlocillin (2 g), gentamicin (0.08 g), amikacin (0.5 g), pefloxaci
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15. A better model of acute pancreatitis for evaluating therapy.
Existing models of acute pancreatitis have limitations to studying novel therapy. Whereas some produce mild self-limited pancreatitis, others result in sudden necrotizing injury. The authors developed an improved model providing homogeneous moderately severe injury by superimposing secretory hyperstimulation on minimal intraductal bile acid exposure. Sprague
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16. Management of necrotizing pancreatitis.
A comprehensive management plan is presented for patients with severe acute pancreatitis. These patients may have pancreatic or peripancreatic necrosis or pancreatic fluid collections. Multiple organ failure often develops in patients with severe pancreatitis. We therefore recommend that all patients with acute pancreatitis be evaluated for pancreatic anatom
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17. Isovolemic hemodilution with dextran 60 as treatment of pancreatic ischemia in acute pancreatitis. Clinical practicability of an experimental concept.
OBJECTIVE: This phase-I study transferred the concept of isovolemic hemodilution, which has been proven beneficial in the treatment of experimental acute pancreatitis to the patient. SUMMARY BACKGROUND DATA: Pancreatic ischemia represents one main mechanism in the pathogenesis of necrotizing pancreatitis. Isovolemic hemodilution with dextran 60 has been show
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18. Intravenous contrast medium aggravates the impairment of pancreatic microcirculation in necrotizing pancreatitis in the rat.
BACKGROUND: Previous reports demonstrated that radiographic contrast medium, as used in contrast-enhanced computed tomography, increases acinar necrosis and mortality in experimental pancreatitis. The authors studied the possibility that these changes may be related to an additional impairment of pancreatic microcirculation. METHODS: Fifty Wistar rats had ac
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19. Indications for surgery in necrotizing pancreatitis.
The decision to operate on a patient with severe acute pancreatitis is often difficult and requires mature clinical judgment. Indications that are widely accepted include to establish the differential diagnosis, when the surgeon is concerned that the symptoms are due to a disease other than pancreatitis for which an operation is mandatory; in persistent and
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20. Decreased mortality of severe acute pancreatitis after proximal cytokine blockade.
OBJECTIVE: This study determined the ability of interleukin-1 receptor antagonist (IL-1ra) to decrease the mortality of experimental acute pancreatitis. The response of the inflammatory cytokine cascade and its subsequent effects on pancreatic morphology were measured to determine the role of these peptides in mediating pancreatic injury. SUMMARY BACKGROUND
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21. Endothelin receptor blockade improves fluid sequestration, pancreatic capillary blood flow, and survival in severe experimental pancreatitis.
OBJECTIVE: To evaluate the effect of a new endothelin receptor antagonist (ET-RA) on the course of severe experimental pancreatitis. BACKGROUND: Endothelin-1 has been shown to reduce regional blood flow in various organs, including the pancreas, and to aggravate cerulein-induced mild pancreatitis. METHODS: Acute necrotizing pancreatitis (ANP) was induced in
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22. Enhanced expression of TGF-betas and their receptors in human acute pancreatitis.
OBJECTIVES: To determine which mechanisms are involved in pancreatic remodeling, repair, and fibrosis after acute necrotizing pancreatitis (NP) in humans. SUMMARY BACKGROUND DATA: Transforming growth factor betas (TGF-betas) are multifunctional polypeptides that have been implicated in the regulation and formation of extracellular matrix and fibrosis. They e