| Research Abstract |
The chemical mediators are secreted from activated platelets. The mediators actually made a play on peripheral vessels and sometimes made remote organ failure even though those materials are instantaneously resolved in blood. We have identified that the microparticles (MP) released from activated platelets were a transporter of the chemical mediators. In order to clarify the release mechanism and physiological meaning of MP the following projects were performed. MP production, platelet P selectin expression, platelet-monocyte binding, and platelet-polymorphonuclear cell binding increased in number in systemic inflammatory syndrome. Anti-P-selectin antibody clearly inhibited platelets-polymorphonuclear cell aggregation. In addition, leukocyte-platelet interaction and endothelial-MP binding were increased in patients with septic condition. Moreover, when the biorheology of the whole blood from septic patients was analyzed with the microarray bloodstream analyzer, the stiffness of white blood cells was increased. The result indicated that migration of white blood cells through the vessel wall was thought to be impaired. The white blood cells, stiffened by inflammation, may be trapped in the local stasis lesion. The platelet and MP bonded to the white blood cells made a new bonding to the other white blood cells. As a result, quite a new mechanism was advocated that start of coagulation accumulates the chemical mediators in inflammatory lesion. Moreover, it was clarified that the cause of activated protein C resistance (APC-R) in venous thrombosis in our country was not due to factor V Leiden gene mutation as was reported in Europe and America. It is not antibodies to phospholipids but anti-protein S antibodies that express APC-R in Japan. And this is the first report in the world (British Journal of Haematology 2002, 118, 577-583,Thromb Haemost 2002, 88, 716-722).
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