Primary portal venopathy in the golden hamster treated with low doses of dimethylnitrosamine.
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.
D000818:Animals; D006224:Cricetinae; D004128:Dimethylnitrosamine; D004195:Disease Models, Animal; D006503:Hepatic Veins / Q000473:pathology*; D008099:Liver / Q000473:pathology; D008297:Male; D008647:Mesocricetus; D010689:Phlebitis / Q000139:chemically induced / Q000473:pathology*; D011169:Portal Vein / Q000473:pathology*; D013927:Thrombosis / Q000139:chemically induced / Q000473:pathology*; D013997:Time Factors
D004128:Dimethylnitrosamine