Thromb Haemost 1987; 58(01): 479
DOI: 10.1055/s-0038-1644573
Abstracts
PLATELET FUNCTIONAL DISORDERS
Schattauer GmbH Stuttgart

MEASUREMENT OF PLATELET IONIZED CALCIUM IN PATIENTS WITH MYELOPROLIFERATIVE DISORDERS BY AEQUORIN METHOD

T Fuzimoto
Department of Internal Medicine, Research Institute for Nuclear Medicine and Biology, Hiroshima Univ. Hiroshima City, JAPAN
,
K Fuzimura
Department of Internal Medicine, Research Institute for Nuclear Medicine and Biology, Hiroshima Univ. Hiroshima City, JAPAN
,
A Kuramoto
Department of Internal Medicine, Research Institute for Nuclear Medicine and Biology, Hiroshima Univ. Hiroshima City, JAPAN
› Author Affiliations
Further Information

Publication History

Publication Date:
23 August 2018 (online)

In myeloproliferative disorders(MPD), bleeding tendency and thrombosis are encountered occasionally in the presence of high platelet counts. It has been reported that there are some abnormalities of membrane glycoprotein or arachidonate metabolism in platelets of MPD. We measured the intracellular change of calcium levels[Cai2+] after stimulation in platelets of the patients with MPD by Aequorin method. Eleven cases of chronic myelogenous leukemia(CML), 7 cases of polycythemia vera(PV), 4 cases of essential thrombocythemiaCET^ and 12 normal adults were studied, and as stimulators 0.5 U/ml thrombin and 2.5 μg/ml collagen were used. In the patients with CML, PV and ET, maximum intracellular calcium level was significantly lower and the reaction period reaching to the peak calcium level(the arrival time) was significantly prolonged than the normals after thrombin stimulation. On collagen stimulation, maximum[Cai2+] level in patient with CML and PV was significantly lower and the arrival time in patient with CML and ET was significantly prolonged than the normals. No correlation was found between maximum [Cai2+] level and maximum aggregation rate or platelet counts in those patients. The increasing rate of intracellular calcium levels after stimulation with A23187 in the presence of various concentration of extracellular calcium was proved lower in CML than in the normal. [45Ca2+] uptake rate into the CML platelets after thrombin stimulation showed lower rate compaired with normals. These results suggest that platelets in patients with MPD have some abnormalities of calcium influx mechanism. We already reported that platelet membrane glycoprotein (GP)IIIa was increased significantly in MPD platelets. The study is going to examine the relationship between this membrane abnormality and impaired calcium influx in MPD.