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[Changes in the liver and brain after portacaval and modified portacaval end-to-side anastomosis: histology, autoradiography and clinical studies].

U Rasenack

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Abstract

Histological studies were done in order to investigate the early and late alterations of the liver and brain in rats after establishment of portacaval anastomosis and modified portacaval anastomosis. The latter procedure allows pancreatic blood to flow into the liver beside portacaval anastomosis. Shunting of portal blood into the systemic circulation through a portacaval anastomosis resulted in hemo-dynamically induced central lobular necrosis of the liver. Necroses and atrophy were less pronounced after modified portacaval anastomosis. The results indicate that optimal perfusion and direct access of hepatotrophic factors are of great importance. Cell necroses in the late phase after portacaval anastomosis are possible due to endotoxinemia. Liver epithelial proliferation was markedly enhanced after complete shunting of portal blood into the systemic circulation. Only minimal proliferation was observed after modified portacaval anastomosis. The results cast doubt on the hypothesis of Starzl that hepatotrophic factors are necessary for all proliferation. Nodular hyperplasia occurring in the late phase of portacaval anastomosis may be due to proliferation of the epithelium. Necroses and injury of ganglia cells as well as alterations of the glia represent the morphological changes in portal-systemic encephalopathy. This is a frequent complication of spontaneous or surgical portacaval collateral circulation. Such changes can also be observed when portacaval anastomosis was constructed in otherwise healthy rats. Increased incorporation rates of 3H-thymidine into the glia were indication for enhanced proliferating activity. Efforts undertaken to maintain the pancreatic venous blood flow to the liver beside portacaval anastomosis resulted in significant diminuation of brain pathology. This happened although the grade of hyperammonemia was virtually identical in both settings. The interpretation is offered that access of the liver to hepatotrophic substances from the pancreas prevents portal-systemic encephalopathy in portacaval anastomosis which is in agreement with data published in the literature. The observation implies that in clinical action exclusively those surgical technics should be used by which the venous blood supply from the pancreas to the liver is maintained.

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What this paper is about

Histological studies were done in order to investigate the early and late alterations of the liver and brain in rats after establishment of portacaval anastomosis and modified portacaval anastomosis. The latter procedure allows pancreatic blood to flow into the liver beside portacaval anastomosis. Shunting of portal blood into the systemic circulation through a portacaval anastomosis resulted in hemo-dynamically induced central lobular necrosis of the liver. Necroses and atrophy were less pronounced after modified portacaval anastomosis. The results indicate that optimal perfusion and direct access of hepatotrophic factors are of great importance. Cell necroses in the late phase after portacaval anastomosis are possible due to endotoxinemia. Liver epithelial proliferation was markedly enhanced after complete shunting of portal blood into the systemic circulation. Only minimal proliferation was observed after modified portacaval anastomosis. The results cast doubt on the hypothesis of Starzl that hepatotrophic factors are necessary for all proliferation. Nodular hyperplasia occurring in the late phase of portacaval anastomosis may be due to proliferation of the epithelium. Necroses and injury of ganglia cells as well as alterations of the glia represent the morphological changes in portal-systemic encephalopathy. This is a frequent complication of spontaneous or surgical portacaval collateral circulation. Such changes can also be observed when portacaval anastomosis was constructed in otherwise healthy rats. Increased incorporation rates of 3H-thymidine into the glia were indication for enhanced proliferating activity. Efforts undertaken to maintain the pancreatic venous blood flow to the liver beside portacaval anastomosis resulted in significant diminuation of brain pathology. This happened although the grade of hyperammonemia was virtually identical in both settings. The interpretation is offered that access of the liver to hepatotrophic substances from the pancreas prevents portal-systemic encephalopathy in portacaval anastomosis which is in agreement with data published in the literature. The observation implies that in clinical action exclusively those surgical technics should be used by which the venous blood supply from the pancreas to the liver is maintained.

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Available abstract

Histological studies were done in order to investigate the early and late alterations of the liver and brain in rats after establishment of portacaval anastomosis and modified portacaval anastomosis. The latter procedure allows pancreatic blood to flow into the liver beside portacaval anastomosis. Shunting of portal blood into the systemic circulation through a portacaval anastomosis resulted in hemo-dynamically induced central lobular necrosis of the liver. Necroses and atrophy were less pronounced after modified portacaval anastomosis. The results indicate that optimal perfusion and direct access of hepatotrophic factors are of great importance. Cell necroses in the late phase after portacaval anastomosis are possible due to endotoxinemia. Liver epithelial proliferation was markedly enhanced after complete shunting of portal blood into the systemic circulation. Only minimal proliferation was observed after modified portacaval anastomosis. The results cast doubt on the hypothesis of Starzl that hepatotrophic factors are necessary for all proliferation. Nodular hyperplasia occurring in the late phase of portacaval anastomosis may be due to proliferation of the epithelium. Necroses and injury of ganglia cells as well as alterations of the glia represent the morphological changes in portal-systemic encephalopathy. This is a frequent complication of spontaneous or surgical portacaval collateral circulation. Such changes can also be observed when portacaval anastomosis was constructed in otherwise healthy rats. Increased incorporation rates of 3H-thymidine into the glia were indication for enhanced proliferating activity. Efforts undertaken to maintain the pancreatic venous blood flow to the liver beside portacaval anastomosis resulted in significant diminuation of brain pathology. This happened although the grade of hyperammonemia was virtually identical in both settings. The interpretation is offered that access of the liver to hepatotrophic substances from the pancreas prevents portal-systemic encephalopathy in portacaval anastomosis which is in agreement with data published in the literature. The observation implies that in clinical action exclusively those surgical technics should be used by which the venous blood supply from the pancreas to the liver is maintained.

Key concepts: Portacaval anastomosis, Portacaval shunt, Anastomosis, Medicine, Encephalopathy, Portal hypertension, Collateral circulation, Surgical anastomosis

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[Changes in the liver and brain after portacaval and modified portacaval end-to-side anastomosis: histology, autoradiography and clinical studies]. — Research Paper | ScholarLens