[Data on humoral regulation of thrombocytopoiesis]. / Nektororye dannye o gumoral'noi reguliatsii trombotsitopoéza.

Biological testing on intact and splenectomized dogs were made to study thrombopoietic activity of the blood in the course of developing drug thrombocytopenia. It is shown that intact dogs' blood contains a thrombopoietin inhibitor inducing the reduction in the mouse platelet count 48 hours after the dog serum injection. In rubomycin model of drug thrombocytopenia, thrombopoietic blood activity increased only after the fall of platelet count by 30% or still more compared to the baseline level. In splenectomized dogs the thrombopoietin inhibitor was not detected, a moderate rise in thrombopoietic activity occurred within 7 weeks. Thrombocytopenia modelling in these conditions requires double cytostatic dose and longer time in spite of less pronounced thrombocytopenia, thrombopoietic activity enhancing to the same degree as without the cytostatic. It is suggested that the spleen produces thrombopoietin inhibitor which links thrombopoietin with megakaryocyte potentiator.

[Role of prostaglandins and cyclic nucleotides in the mechanism of development of drug-induced thrombocytopenia]. / Rol' prostaglandinov i tsiklicheskikh nukleotidov v mekhanizme razvitiia medikamentoznoi trombotsitopenii.

The experiments on dogs have shown that at the moment of maximal thrombocytopenia, induced by using of 0.7 mg/kg rubomycin intravenous daily during 5 days, there was a sharp increase in cAMP concentration, while the content of prostaglandin E group and F2 alpha in blood decreased. Concentration of cGMP began to increase by the 10th day. We can arrive at the opinion that the rubomycin acts on the receptors of hemopoietic precursor cells' membrane. This causes the activation of adenylate-cyclase, which stimulates the formation of cAMP, causing cells' proliferation depression. This mechanism may be regarded as the restoration reaction of megakaryocyte-thrombocyte system.