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推测暂时性脑缺血发作(TIA)是因血栓栓塞所致,它与血小板参与:血小板-纤维蛋白原聚合物的产生、缺血区的止血、和动脉粥样硬化形成有关。因此认为,能抑制血小板参与血栓或动脉粥样硬化形成的药物,有助于防止发作。许多不同的刺激物可引起血小板改变形状,粘附于异常的内皮表面或互相粘在一起,并分泌许多不同的“释放反应”物质。胶原、肾上腺素和二磷酸腺甙(ADP)可刺激血小板释放三磷酸腺甙(ATP)以及附加的ADP、5-羟色胺、钙和血小板因子4.凝血酶是一种更强的刺激物,可引起其它成分如纤维蛋白原和溶酶体水解酶释放。另外,血小板可排出花生四
It is hypothesized that transient ischemic attack (TIA) is caused by thromboembolism and is associated with platelet involvement: platelet-fibrinogen polymer production, hemostasis in the ischemic area, and atherosclerosis. Therefore, it is thought that drugs that inhibit platelet involvement in the formation of thrombus or atherosclerosis help to prevent the onset of seizures. Many different stimuli can cause platelets to change shape, stick to abnormal endothelial surfaces or stick together and secrete many different “release-response” substances. Collagen, epinephrine and adenosine diphosphate (ADP) stimulate the release of adenosine triphosphate (ATP) from platelets and additional ADP, serotonin, calcium and platelet factor 4. Thrombin is a stronger stimulant and may Causing other components such as fibrinogen and lysosomal hydrolase release. In addition, platelets can be discharged four peanuts