Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological and biochemical changes were observed in the pancreas and serum of rats after the intraperitoneal administration of selenomethionine, sodium selenite and methionine. Selenomethionine caused rapidly developing acinar cell necrosis. The first pathological changes were mitochondrial swelling and flocculent densities, and dilatation of cisternae of the endoplasmic reticulum. Zymogen granules appeared disrupted only in disintegrated acinar cells. Signs of autodigestive pancreatic inflammation with fat necrosis, elevation of pancreatic phospholipase A2 and serum amylase activities, as well as pulmonary oedema were present. Sodium selenite caused similar histologic changes to those produced by selenomethionine, but no changes were seen after methionine administration. Destruction of pancreatic acinar cells by an intraductal oleic acid injection that resulted in exocrine atrophy did not prevent systemic selenomethionine toxicity. Our results show that selenomethionine causes pancreatic acinar cell necrosis and that intracellular transport and storage of digestive enzymes is not primarily altered by this chemical.
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PMID:Pancreatic acinar cell necrosis with intact storage of digestive enzymes in selenomethionine treated rats. 197 21

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 experimental study was undertaken to elucidate the destruction of pulmonary surfactant in acute pancreatitis using the lung pressure volume curve (P-V curve). Acute hemorrhagic pancreatitis was induced in mongrel dogs by a retrograde injection of Na-taurocholate into the main pancreatic duct. Pulmonary surface tension was measured by P-V curve and the effect of PLA2 on pulmonary surfactant was assessed by the ratio of lysolecithin and lecithin, which are essential components of pulmonary surfactant (Ly/Le) in lung wash. Extravascular lung water volume (Ww/Dw) and blood gases were also measured. The value of Ly/Le and serum PLA2 rose significantly from the 3rd hour. On the contrary, no significant differences were seen on P-V curve until the 12th hour but after 20 hours surface tension increased significantly. Ww/Dw and A-aDO2 increased after 3 and 12 hours, respectively. These findings, the degradation of lecithin and the elevation of surface tension accompanied with an increase of serum PLA2, suggest that pulmonary surfactant is destroyed in severe acute pancreatitis, and that the increased capillary permeability of the lung precedes the deterioration of surface tension as the cause of pulmonary insufficiency.
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PMID:[Experimental study on the pathogenesis of pulmonary insufficiency in acute pancreatitis and changes in the pulmonary surfactant]. 322 26