血栓与止血检验北医课件.ppt

* * Within seconds after vascular injury platelets accumulate and adhere to the damaged vessel wall where they become activated, triggering the release of prothrombotic factors such as thromboxane A2 and ADP through platelet dense granules. This release of activators propagates platelet activation, which leads to subsequent aggregation. This activation of platelets represents a continuing assault on lesions throughout the vasculature. The key to chronic control of platelet aggregation is to manage this ongoing rapid onset of platelet ACTIVATION. ? References: ? Gibbons, J.M. 2004. Platelet adhesion signaling and the regulation of thrombus formation. Journal of Cell Science. 117: 3415-3425. ? Woulfe, D., Yang, J., Brass, L. 2001. ADP and platelets: the end of the beginning. J Clin. Invest. 107: 1503-1505. ? Faxon, DP et. 2004. Atherosclerotic Vascular Disease Conference Writing Group III: Pathophysiology. Circulation.109: 2617-2625. * Unactivated platelets are rapidly recruited to the site of injury where glycoprotein mediated binding to the exposed tissue elements stimulates platelet signaling which results in a shape change from the usual disk-like form to spheres with extended pseudopodia, thereby enhancing the ability of the platelets to interact with each other and with the subendothelial surface. ? Slide Navigation: You may click on the second image which includes the platelets to view a close up of the shape change the platelet undergoes with activation. Click inside the circle to view an actual photo of activated platelets. References: ? Gibbons, J.M. 2004. Platelet adhesion signaling and the regulation of thrombus formation. Journal of Cell Science. 117: 3415-3425. EM photo courtesy of Dr. Ogawa at Sankyo Co., Ltd., Tokyo. * Platelets now begin to release numerous prothrombotic activators with platelet activation becoming highly amplified. Preformed ADP is released from platelet dense granules. Thromboxane A2 is generated f