SummaryExtracts from dog livers which had been regenerating for 24, 48, and 72 h after hepatectomy were infused for 6 h into the left portal vein of animals which had fresh portacaval shunts (Eck fistula) and which were killed 2 and 3 days later. The brief exposure to the 48-h and especially the 72-h regenerating liver extracts induced a delayed proliferative response predominantly in the left liver lobes, with a slight spillover effect to the right liver lobes but none to the kidney. The response reached its peak 3 days later. In the left but not the right liver lobes, both the 48-h and the 72-h regenerating liver extract reversed the atrophy ordinarily caused by Eck fistula in 3 days and partly prevented the ultrastructural hepatocyte deterioration characteristic of Eck fistula. The active liver extracts apparently contained a growth-control factor or factors which is (are) not insulin or glucagon.

Forty-four percent and 72% hepatectomy were carried out in dogs and the animals were sacrificed for biochemical and pathologic studies from 0.5 to 6 days later. Compensatory hypertrophy and hyperplasia ("regeneration") were evident within 1 day, reached a maximum in 3 days, and were almost complete by 6 days. Coincident with the histologic events of regeneration were decreases in responsiveness of receptor adenyl cyclase to glucagon stimulation, increases of cyclic AMP, inconsistent changes in plasma insulin, and increases in plasma glucagon. These studies have standardized hepatic resection in dogs and they have focused attention upon some possible mechanisms that will require further study.

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Hepatic cholesterol synthesis, hepatic cyclic AMP, and portal and peripheral insulin and glucagon levels were investigated in nine dogs and three baboons after complete portacaval shunt. Cholesterol synthesis as measured with acetate incorporation was reduced in both species. Hepatic cyclic AMP increased in dogs. Changes in portal and systemic insulin were inconsistent, but hyper-glucagonemia occurred regularly. Diminished hepatic cholesterol synthesis is apparently one factor, although probably not the only one, in the antilipidemic effect of portacaval shunt. This altered cholesterol metabolism may be due to a change in the hormonal environment of the liver caused by portal diversion.

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