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The concentration of hepatic storage iron (nonheme iron) is increased by 62.3 percent after portacaval shunting in dogs. Such increase is presumably due to the presence of an increased amount of hemosiderin, as observed on microscopic examination of sections of liver. Because of the known reduction of liver volume and the suspected reduction of hepatic ferritin concentration after shunting, the increase in the concentration of hepatic storage iron is a reflection of the increase in hepatic hemosiderin concentration. Hepatic storage iron concentration is not an accurate index of either the increase in hepatic storage iron content or hepatic hemosiderin content.
The serum iron concentration declines rapidly from 154 γ to 60 γ per 100 ml. after portacaval shunt and returns slowly to the level prior to operation, while the serum iron-binding capacity rises slowly from 186 to 238 γ per 100 ml. after portacaval shunt. The osmotic fragility and half-life of the red cells (Cr51) do not change significantly after portacaval shunt.
The ratio of the rib-marrow space occupied by fat compared to that occupied by hematopoietic cells is increased from 1:2.3 in dogs undergoing thoracic and orthopedic operations, to 2.3:1 in dogs undergoing portacaval shunt operations. A selective depression of erythropoiesis and arrest in red cell maturation do not occur.
These results suggest that hematopoiesis is generally depressed as a result of the portacaval shunt, and that iron previously used in the production of hemoglobin is stored in the liver as hemosiderin. The significance of these findings relative to the reported human cases of hemochromatosis after portal-systemic shunting is discussed.
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Received: March 24, 1964
© 1965 Published by Elsevier Inc.