抄録
Introduction. Atherothrombosis, including myocardial infarction and ischemic stroke, is a leading cause of death in the modern world. Platelet, forming thrombi at site of ruptured or disrupted atherosclerotic plaque, play crucial role in the onset of atherothrombosis. Mechanism of platelet thrombus formation under blood flow condition may not be the same as platelet aggregation under static conditions. Method. Whole blood, containing platelets rendered fluorescent by addition of mepacrine or calcium sensitive dye of Fluo-3, was perfused on the immobilized collagen fibrils at various shear rate conditions. Two-dimensional and three-dimensional growth of platelet thrombi on the collagen fibrils were detected by epi-fluorescent video-microscpy and ultra-fast laser confocal miscroscope equipped with piezo-motor control unit, respectively, Real time visualization of intra-cytoplasmic calcium ion concentration was also achieved with the use of laser confocal microscopy. Results. Unlike platelet aggregation under static condition, platelet thrombus growth on the collagen fibrils under blood flow conditions was markedly inhibited by blocking von Willebrand factor binding with glycoprotein Ibα, ADP binding with P2Y12 ADP receptor, and so on. Our results also revealed that cyclic increase in intracytoplsmic calcium ion concentration was abolished when P2Y12 was blocked. Collagen and thrombin also play important roles in the growth of platelet thrombi. Conclusion. Mechanism of platelet thrombus formation under blood flow conditions are different from that of platelet aggregation under static condition. [J Physiol Sci. 2006;56 Suppl:S49]
