Serum thrombopoietic activity following administration of vinblastine.
A possible role of humoral factors in the pathogenesis of vinblastine-induced thrombocytosis was examined. The thrombopoietic activity in serum of experimental animals was tested for its ability to stimulate the incorporation of 75-Se-selonemethionine into platelets of thrombocythaemic mice. The administration of low doses (0.1--0.5 mg/kg body wt.) of vinblastine to rabbits caused a significant increase in serum thrombopoietic activity. Higher doses of vinblastine (1--5 mg/kg body wt.) also increased the serum thrombopoietic activity, but this increase was preceded by a transient drop in the platelet count of peripheral blood. This thrombocytopenia could have been a stimulus for an increase in thrombopoietic activity, through a compensatory feedback mechanism. The vinblastine-induced increase in thrombopoietic activity was abolished by bilateral nephrectomy but not by bilateral ureteral ligation. These data suggest that kidney tissue may be a major source of the serum thrombopoietic factors.
D000818:Animals; D001681:Biological Assay; D001772:Blood Cell Count; D005260:Female; D006023:Glycoproteins; D007668:Kidney / Q000502:physiology*; D008297:Male; D011817:Rabbits; D013922:Thrombocytosis / Q000139:chemically induced*; D013926:Thrombopoietin; D013997:Time Factors; D014513:Ureter / Q000502:physiology; D014747:Vinblastine / Q000008:administration & dosage / Q000494:pharmacology*
D006023:Glycoproteins; D014747:Vinblastine; D013926:Thrombopoietin