Puslapis 1 nuo 1107 rezultatus
Gastric wall edema has not been reported as a complication of acute pancreatitis in dogs.To describe the ultrasonographic features of gastric wall thickening in dogs with acute pancreatitis.Fourteen dogs with ultrasonographic The complement cascade is activated in humans and animals with acute pancreatitis. Activation of complement component C5 liberates C5a, C5a-desarg, and terminal complement complexes (TCCs) that increase capillary permeability, edema, and leukocyte chemotaxis at injured sites. Complement activation
The authors report a case of severe hypertriglyceridemia (148.5 mmol/l) in a 27-year-old woman admitted for coma of unknown origin. Initial investigations revealed ketoacidosis, pancreatitis and noncardiogenic pulmonary edema. The diabetes was unknown. Ketoacidosis was rapidly controlled. The
Pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and
OBJECTIVE
To study MRI findings of abdominal wall edema (AWE) in acute pancreatitis as well as correlations between AWE and the severity of acute pancreatitis according to the MR severity index (MRSI) and the Acute Physiology And Chronic Healthy Evaluation III (APACHE III) scoring system.
METHODS
A
Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was
The large availability of salicylic acid products makes them an often encountered source of poisoning in the emergency department. Even though in most cases the prognosis is good, with a low incidence of long-term morbidity and mortality, complications do occur, and some of those can be life
Previously we reported that prior administration of lipopolysaccharide (LPS) mitigates subsequently produced cerulein (Cn) pancreatitis. To clarify the mechanism further, the pathological features of Cn pancreatitis were examined in detail after treating rats with very low doses of LPS. LPS
Since oxygen free radicals and lipid peroxidation have been implicated in the pathogenesis of an early stage of acute pancreatitis, we examined whether melatonin, a recently discovered free-radical scavenger, could attenuate pancreatic injury in Sprague-Dawley rats with cerulein-induced
Acute pulmonary edema appeared 3 or more days after the onset of acute pancreatitis in 7 patients, an approximate incidence of 8%. The severity of pancreatitis in these patients was characterized by massive requirements for intravenous colloid and by marked hypocalcemia. In addition, at least 5 of
For experimental analysis of pathogenesis of acute pancreatitis a suitable animal model is necessary. The pancreatic (juice) edema and an alteration of cellular energy metabolism are important pathogenetic factors. A partial intrapancreatic edema was induced by stimulating secretion against
Acute hemorrhagic pancreatitis was induced in rats by injecting sodium taurocholate into the common biliopancreatic duct. The extent of pancreatic necrosis was quantified in histological sections during the course of the disease. The proportion of necrotic acini was low, although the amount of
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
The present study was done to determine the influence of single oral, intravenous and intraperitoneal ethanol administration at pre-existing pancreatic juice edema on frequency and severity of acute pancreatitis (AP). The rats were divided into six control (isolated treatment) and five study groups
Acute pancreatitis is characterized by hyperamylasemia, pancreatic edema, and the presence of activated digestive enzymes within the pancreas. The secretagogue-induced model of acute pancreatitis is also characterized by pancreatic acinar cell vacuolation, subcellular redistribution of lysosomal