Compensatory hyperplasia in the rat liver as a result of cytoplasmic atrophy.
A protracted process of hepatocyte atrophy was induced in the anterior lobes of the rat liver by portal vein ligation (PVL), and within 3 days the combination of atrophy in the anterior lobes and compensatory hyperplasia of the posterior lobes had resulted in the anterior lobes comprising only about 20% of the total liver weight. Apart from an initial fall in the total liver weight due to atrophy of the anterior lobes without any corresponding growth reaction in the posterior lobes, the total liver weight remained close to normal throughout the first 3 days. Surprisingly, increases in posterior lobe DNA synthesis after PVL were triggered almost as rapidly (15-18 h post-operatively) as occurs after anterior lobe resection, though subsequently the level of proliferative activity was generally lower than is found after partial hepatectomy. The rapidity of the proliferative response to PVL suggests the proliferative signal is generated by a minimal cytoplasmic deficit and/or the increased rate of portal blood perfusion.
D000818:Animals; D001284:Atrophy / Q000473:pathology; D003593:Cytoplasm / Q000473:pathology; D004247:DNA / Q000096:biosynthesis; D006965:Hyperplasia / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008026:Ligation; D008099:Liver / Q000098:blood supply / Q000473:pathology*; D008297:Male; D008940:Mitotic Index; D009929:Organ Size; D011169:Portal Vein; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D004247:DNA