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lysolecithin/hemorrhage

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10 結果

Experimental pancreatitis in the rat. The role of phospholipase A in sodium taurocholate-induced acute haemorrhagic pancreatitis.

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Acute haemorrhagic pancreatitis was induced in rats by injecting 0.2 ml of 5% (92.9 mmol/l) aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lysolecithin was separated from the pancreatic homogenate by thin-layer chromatography and quantified by phosphorus determination.

Lysolecithin concentration in pancreatic tissue during therapy with phospholipase A2-inhibitors in acute necrotizing pancreatitis.

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Four hours after hemorrhagic necrotizing pancreatitis was induced in experimental animals the concentration of lysolecithin in pancreatic tissue rose (p = 0.0025). Parenteral administration of unspecific inhibitors of phospholipase A2, such as chlorpromazine, gabexat mesilat and CaNa2 EDTA, can

Duodenogastric reflux of lysolecithin in the pathogenesis of experimental porcine stress ulceration.

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The role of duodenogastric reflux of lysolecithin, a normal constituent of duodenal juice, in the pathogenesis of gastric stress ulcerations was investigated with a swine shock-ulcer model. Twenty-seven piglets, weighing 8 to 12 kilograms, were used. In an intact animal, the average concentration of
Acute experimental pancreatitis was induced by retrograde injection of 0.15 ml of 0.8% lysolecithin into the pancreatic duct of Wistar rats. This procedure was always followed by severe necrosis of pancreatic parenchyma, bloody ascites and numerous fat necroses in the abdominal cavity.

[Phospholipase A2 inhibitors in hemorrhagic-necrotizing pancreatitis. Animal experiment evaluation of a new treatment concept].

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In mongrel dogs with induced pancreatitis we studied the effects of the nonspecific phospholipase A2-inhibitors chlorpromazine, gabexate mesilate and CaNa2EDTA on the course of pancreatogenic shock and the intrapancreatic lysolecithin production. The local level of lysolecithine the metabolite of

[Experimental study on the pathogenesis of pulmonary insufficiency in acute pancreatitis and changes in the pulmonary surfactant].

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Serious pulmonary complications are often associated with acute pancreatitis. The destruction of pulmonary surfactant by the action of pancreatic phospholipase A2 (PLA2), together with pulmonary edema, is considered an important etiopathogenic factor of acute respiratory insufficiency. This

The multimolecular cascade of spinal cord injury. Studies on prostanoids, calcium, and proteinases.

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Experimental spinal cord injury in animals induced by weight drop produces neurological deficit and paralysis. Correlation of the progressive morphological changes in the lesion by both light and electron microscopy with the biochemical alterations revealed ischemia, edema, hemorrhage, tissue

Investigations into various pancreatic enzymes.

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The effects of several pancreatic enzymes on living tissue incapable of autodigestion were studied to analyse elements of the "pluralistic events of acute hemorrhagic pancreatitis" (Becker 1981). Phospholipase A2 induces (via toxic lysolecithin) cytotoxic necrosis in the testis; elastase (via

Experimental pancreatitis in the rat. Changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis.

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Acute haemorrhagic pancreatitis was induced in rats by injecting aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lecithin and lysolecithin were separated from pulmonary homogenate by thin layer chromatography and quantified by phosphorus determination. The ratio of

[Lipids in serum and cerebrospinal fluid in acute cerebrovascular disorders].

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The cholesterol and lipoid phosphorus levels in the serum and liquor' cerebrospinalis were studied in 40 patients suffering from ischaemic cerebral lesions. A chromatographic determination was also performed for eight sub-fractions of polar and neutral fats (lysolecithin, sphingomyelin, lecithin,
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