抄録
The sequestration of erythrocytes in rats was studied using an isologous 51Cr-labeled population of either normal or N-ethyl-maleimide (NEM) treated red cells.
The spleen sequestered the damaged red cells selectively, while the liver compensated and overshot the sequestration for spleen after splenectomy. The sequestering response in liver increased gradually reaching a maximum level around 8 weeks after splenectomy and then declining toward the control level. These compensatory responses in liver were not observed in rats fed a low-protein diet, which indicated that the proliferative response imposed on liver by an extra work after splenectomy was not stimulated in the rats fed a low-protein diet.
Splenectomy prolonged erythrocyte survival and reduced the osmotic fragility of normal red cells, but the compensatory increase in sequestration of damaged red cells in liver did not alter the survival and osmotic fragility of normal red cells of the rat. This fact indicates that the increased sequestration of reticuloendothelial cells in liver is basically reparative, and it is impossible to compensate for the absence of the spleen because of an inability to duplicate certain anatomic features peculiar to the spleen.
