Tschoepe D, Rauch U, Schwippert B
Diabetes Research Institute, Heinrich Heine University of Duesseldorf, Germany.
Horm Metab Res. 1997 Dec;29(12):631-5. doi: 10.1055/s-2007-979115.
The physiological meaning of platelets has been best documented for acute coronary syndromes where platelets act as "first responsive elements" triggering the final occlusive thrombus after plaque rupture has occurred. This situation is particularly relevant for patients with NIDDM-type diabetes regularly showing complicated plaque architecture. Predictive power for acute ischemic events e.g. following angioplasty has been proven, and this has dominated the attention exclusively towards the hemostatic function of platelets. Meanwhile, a variety of particularly important platelet features have been identified: a) promotion of liquid phase coagulation; b) regulation of the local vascular tone; c) active modulation of tissue modeling at lesion sites; d) adhesion molecule-mediated communication with a variety of corpuscular blood (and non-blood cells). With emerging recognition of the latter role, the pathophysiological scope of platelets exceeds the well-established role as microemboli, local atherosclerosis amplifiers and triggers of gross thrombosis. In diabetes mellitus of either type, increased populations of circulating platelets have been identified expressing activation dependent adhesion molecules such as activated alpha 2 beta 3 (GPIIbIIIa), lysosomal GP53, thrombospondin or, perhaps most importantly "P-selectin" (CD62 p). This suggests that these adhesion molecules among others can also mediate platelet-leukocyte interactions potentially resulting in inflammatory tissue damaging processes in addition to the immanent tendency towards (micro-)thrombosis. This review works out a more general view on the meaning of platelet activation beyond hemostaseology and updates the actual knowledge of platelet-leukocyte communication checkpoints with particular reference to the diabetic state outlining new pharmacological concepts for intervention.
血小板的生理意义在急性冠状动脉综合征中得到了最充分的记录，在这种情况下，血小板作为“第一反应元件”，在斑块破裂后触发最终的闭塞性血栓。这种情况在经常表现出复杂斑块结构的非胰岛素依赖型糖尿病（NIDDM）患者中尤为相关。例如，血管成形术后急性缺血事件的预测能力已得到证实，这使得人们的注意力完全集中在血小板的止血功能上。与此同时，已经确定了血小板的各种特别重要的特征：a）促进液相凝血；b）调节局部血管张力；c）积极调节病变部位的组织重塑；d）通过粘附分子与各种血细胞（和非血细胞）进行通讯。随着对血小板后一种作用的认识不断增加，血小板的病理生理作用范围超出了其作为微栓子、局部动脉粥样硬化放大器和大血栓形成触发因素的既定作用。在任何一种类型的糖尿病中，都已发现循环血小板数量增加，这些血小板表达激活依赖性粘附分子，如活化的α2β3（糖蛋白IIbIIIa）、溶酶体糖蛋白53、血小板反应蛋白，或者可能最重要的是“P-选择素”（CD62 p）。这表明，除了内在的（微）血栓形成倾向外，这些粘附分子还可能介导血小板与白细胞的相互作用，从而潜在地导致炎症性组织损伤过程。这篇综述对血小板激活在止血学之外的意义提出了更全面的观点，并更新了血小板与白细胞通讯检查点的实际知识，特别参考了糖尿病状态，概述了新的干预药理学概念。
