Biological testing on intact and splenectomized dogs were made to stud
y thrombopoietic activity of the blood in the course of developing dru
g thrombocytopenia. It is shown that intact dogs' blood contains athro
mbopoietin inhibitor inducing the reduction in the mouse platelet coun
t 48 hours after the dog serum injection. In rubomycin model of drug t
hrombocytopenia, thrombopoietic blood activity increased only after th
e fall of platelet count by 30% or still more compared to the baseline
level. In splenectomized dogs the thrombopoietin inhibitor was not de
tected, a moderate rise in thrombopoietic activity occurred within 7 w
eeks. Thrombocytopenia modelling in these conditions requires double c
ytostatic dose and longer time in spite of less pronounced thrombocyto
penia, thrombopoietic activity enhancing to the same degree as without
the cytostatic. It is suggested that the spleen produces thrombopoiet
in inhibitor which links thrombopoietin with megakaryocyte potentiator
.