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Society of University Surgeons| Volume 52, ISSUE 1, P88-102, July 1962

Liver regeneration following portacaval shunt

DOI:https://doi.org/10.5555/uri:pii:0039606062902878
Liver regeneration following portacaval shunt
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      Abstract

      The results of this study indicate that the liver has not lost its capacity to regenerate following portacaval shunt, and the degree of restoration is not significantly different from that observed in intact animals following partial hepatectomy. Such conclusions result from the use of shunt animals, rather than intact normal animals, as suitable controls for the assessment of regeneration. The effect upon the liver of portacaval shunt alone has thus been distinguished from that following combined shunt and partial hepatectomy.
      Considerable atrophy results from restriction of portal blood flow. Such livers are capable of restoration of hepatic mass and protein, and, as evidenced by mitotic counts and incorporation of P32 into DNA, parenchymal cells undergo division in a fashion comparable to that observed following liver resection in animals with an intact circulation. Contrary to the reports of others, it appears from these findings that portal blood, or blood per se, traversing the liver via the portal circulation, is not so much a prerequisite for hepatic restoration as it is for the inhibition of hepatic atrophy.
      Liver atrophy was slight after side-to-side shunt, as compared with that after end-to-side shunt. The degree of hepatic (and protein) restoration following partial resection was, however, similar in both groups (65 per cent and 61 per cent). Possible clinical significance of these findings is being entertained.
      No evidence was obtained to support the importance of a humoral factor in the process of liver regeneration in portacaval shunt animals. The injection of plasma from hepatectomized rats into single shunt animals and partial hepatectomy, with or without antecedent portacaval shunt in one member of a parabiotic pair, failed to disclose significant differences in the number of mitoses or DNA-P specific activity of liver compatible with the presence of such a factor.
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      Article info

      Footnotes

      ☆Supported by United States Public Health Service Grants No. A-4651 and No. A-369.

      ☆☆Read at the Twenty-third Annual Meeting of the Society of University Surgeons, Cleveland, Ohio, Feb. 8–10, 1962.

      Identification

      DOI: https://doi.org/10.5555/uri:pii:0039606062902878

      Copyright

      © 1962 Published by Elsevier Inc.

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