Liver regeneration after portacaval transportation in rats

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      General recognition of the presence of a specific hepatotrophic factor in portal blood that is necessary for liver regeneration was delayed by two major problems. First, there was a long period of confusion regarding liver atrophy, liver hypertrophy, and cellular hyperplasia. Second, because only exposure to other liver tissue destroys the hepatotrophic activity, all of the studies that were based on bypassing the portal blood into the systemic circulation merely diluted the active substance, which still was available to the hepatocytes by recirculation through the hepatic artery. These problems have been resolved by the development of more sophisticated methods by which to assay liver regeneration and by the introduction of the double liver model to study regeneration. During the time when liver weight alone was used to assess regeneration, the regenerative capacity of the liver was reported to be much greater after portacaval transposition than after end-to-side portacaval shunt, a finding that is inconsistent with current knowledge of the hepatotrophic portal blood factor. To re-evaluate the effect on liver regeneration of providing a compensatory systemic venous inflow after complete portal diversion, 40 partially hepatectomized inbred rats which had previously undergone either a sham operation and end-to-side portacaval shunt or a portacaval transposition were compared on the basis of six separate criteria of regeneration. Alf of the livers actively regenerated and no significant advantage of providing a substitute systemic venous inflow to the liver could be detected by any of the criteria.
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