Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The liver of Syrian hamsters was studied after exposure to dimethylnitrosamine (DMN) in drinking water for, respectively, 8, 12 and 16 weeks. One additional group of animals was offered DMN for 8 weeks, but maintained for further 8 weeks after removal of the compound. The changes consisted of a narrowing portal venopathy, probably arising, initially, from toxic pylephlebitis, being followed by widespread subendothelial prolapse of hepatocytes encroaching upon the lumen of terminal hepatic veins, which generally were free of inflammatory fibrosing lesions. The venous lesions were unrelated to malignant processes in the biliary duct system, which occurred after 16 weeks. Dilatation of sinusoids and small venules was associated with the presence of prolapsed hepatocytes around their openings into involved larger veins. At the end of 12 and 16 weeks of continuous ingestion of DMN, but also where the agent was withdrawn already at 8 weeks, phlebectasis and transitional stages in the formation of teleangiactatic type of peliosis were demonstrated, probably resulting from progressively impeded blood flow due to partial occlusion by prolapsed hepatocytes in terminal veins. The mechanism enabling hepatocytes to penetrate the venous wall was not clarified. There was no indication of invasive malignancy. Hepatocyte prolapse appeared more likely to result from some unknown mechanism of benign infiltration, promoted by regenerative stimulation. This may have been initiated by mild persistent ischemia due to the demonstrated portal venopathy. No endothelial hyperplasia was seen at any stage of the experiments thus eliminating the probability of peliosis being a source of vascular neoplasia, which has previously been described following more prolonged exposure to DMN. Certain parallelisms of the experimental results with hepatic vascular lesions in man subjected to drug therapy are discussed.
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PMID:Venoocclusive disease of the liver and phlebectatic peliosis in the golden hamster exposed to dimethylnitrosamine. 373 74

Ingestion of dimethylnitrosamine in a low dose and for a limited period by hamsters resulted in primary intrahepatic pylephlebitis. The process began at 24 h and progressed within 2-4 weeks to narrowing and, eventually, to partial obstruction of the portal bed. The lesions were characterized by endothelial necrosis followed by infiltrations of lymphoid cells extending into the portal tracts. Superficial lesions of terminal hepatic veins and parenchymal changes occurred only after a lapse of, respectively, 2 and 4 weeks when restrictions of portal blood had been assumed. The parenchymal changes consisted of regional regenerative hyperplasia accompanied by subendothelial prolapse of hepatocytes into the wall of terminal veins. The lesions of the portal veins persisted for a prolonged period of time after the exposure to dimethylnitrosamine had ceased. These findings, associated with characteristic histological aspects, suggested secondary immune reaction following the initial toxic pylephlebitis. The possible relevance of the experimental results to understanding the nature of endemic portal venopathy in man is discussed with regard to pathogenesis and etiology.
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PMID:Primary portal venopathy in the golden hamster treated with low doses of dimethylnitrosamine. 648 85