On Wistar rats splenic involvement into the regulation of erythropoiesis was studied. Splenomegaly was reproduced for this both by
ligation of splenic veins and transfusion of suspension of washed erythrocytes that leaded to the pronounced increase in the size of the
spleen which has reserved the part of erythrocytes. It has been shown that in both cases the inhibition of erythropoiesis takes place due to
the appearance of the active inhibitor in plasma: the injection of such plasma reduces the hematopoietic activity of intact rats-recipients.
It is assumed that the inhibitor depresses the formation of blood by reducing the production of erythropoietin by the kidneys. We believe
that the inhibiting effect is caused by serotonin, which concentration in blood plasma was increased. The inhibiting effect of serotonin
is evidenced by its increase in those layers of the kidneys, which are structures that synthesize erythropoietin. Indirect confi rmation of
serotonin’s participation in the inhibition of hematopoiesis may be the clinical data about decreased platelet count, which are apparently
destroyed in the spleen (platelets contain a lot of serotonin), in patients with splenomegaly. We have shown that if you deprive the
spleen of the possibility to deposit the excess of transfused red blood cells by preliminary sheathing it with capron, the appearance of
erythropoiesis inhibitory factor (serotonin) doesn’t happen. Thus, we believe that the normal activation of the spleen (hypersplenism)
takes place in case of secondary splenomegaly in patients with the cirrhosis of the liver, it consists in the regulation of erythropoiesis
through its function of depositary. And we propose to call this function of normal spleen «splenism»