[Heparin and blood platelets].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Komarnicki.
Explore the source record for details and available documents.
In 22 patients with acute myeloid leukaemia (17 cases of myeloblastic leukaemia, 4 cases of myelomonocytic leukaemia and 1 case of undifferentiated-cell leukaemia) platelets were isolated from the plasma by the method of Nicholls and Hampton as modified by Levy-Toledano by centrifugation in albumin gradient. The aim of platelet isolation was their "concentration" in cases of thrombocytopenia to values making possible aggregation tests, and platelet separation from the influence of plasma factors. Then aggregation of isolated platelets caused by ADP was studied. In 16 out of 22 patients a fall of aggregation was observed, with the mean values of aggregation rate and intensity were significantly lower. Parallelly done determinations of aggregating activity released from the platelets by thrombin showed lower values as compared with platelets from healthy subjects. In might be thought, in this connection, that the demonstrated reduction of isolated platelets is associated with a diminution of the nucleotide pool or disturbances of the platelet release reaction. The disturbances of the platelet release reaction. The disturbances of aggregation of isolated platelets and reduction of the aggregating activity were most pronounced in acute myelomonocytic leukaemia.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
An effect of a standard heparin preparation on the interaction between blood platelets and collagen has been investigated. The experiments have shown, that the addition of heparin in the concentration of 0.3; 0.6 or 0.9 IU/mL did not change the interaction between blood platelets and collagen. Such interaction increased, when heparin concentration was 1,2 IU/mL, and remained unchanged despite the further increase in heparin concentration. The authors suggest that such a course of this interaction results from the stimulating action of heparin added in adequate concentration on protein release from platelet alpha granulations--which bound GP II b/III a complex with collagen.