Davì G, Traina M, Novo S, Pinto A, Piraino G L, Marano G, Alfano R
G Ital Cardiol. 1981;11(9):1238-41.
Platelets are thought to be involved in the initiation and propagation of arterial and venous thrombi. A new formation of platelet thrombus in a coronary artery has been implicated in the genesis and extension of myocardial infarction. Experimental evidence suggests that platelet aggregates may be responsible for occlusion of small coronary arteries and subsequent ischemia. Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanisms - operating at the microenvironment level from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Although myocardial infarction is usually associated with arteriographic evidence of atherosclerotic coronary obstruction, examples of infarction in the absence of coronary artery disease have been reported. ARterial thrombosis, small vessel coronary disease and arterial spasm are several possibilities that have been described. Recently in some cases of myocardial infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets during myocardial ischemia as an increase of prostaglandin synthesis, like prostacyclin, is stimulated by ischemia and hypoxia. The local release of these substance may modify the myocardial cell viability and regional blood flow. The aim of the present study was to investigate some changes in platelet function in relation to the time stimulated with thrombin. The tests showed, in the first three days, an augmented release of BTG levels with a platelet "exhaustion", demonstrated by a reduced formation of MDA by platelets changing to a state of hyperactivity, with a maximal production of MDA in 10th-15th day.
血小板被认为参与动脉和静脉血栓的形成与传播。冠状动脉中血小板血栓的新形成与心肌梗死的发生和扩展有关。实验证据表明血小板聚集体可能是小冠状动脉阻塞及随后缺血的原因。在特定患者中,心肌梗死的血栓形成成分是原发性还是继发性的,血小板功能改变均可影响许多机制——这些机制在微环境水平起作用,而血栓性病变是否发展或向较小的心肌血管发送血小板栓子取决于此微环境。虽然心肌梗死通常与冠状动脉粥样硬化阻塞的血管造影证据相关,但也有报道称在无冠状动脉疾病的情况下发生梗死的病例。动脉血栓形成、小血管冠状动脉疾病和动脉痉挛是已被描述的几种可能情况。最近在一些心肌梗死病例中,血管造影显示有冠状动脉痉挛;血栓素,即血管收缩和血小板聚集物质,由血小板释放;在心肌缺血期间,由于缺血和缺氧刺激前列腺素合成增加,如前列环素,血小板会释放血栓素、血管收缩和血小板聚集物质。这些物质的局部释放可能会改变心肌细胞活力和局部血流。本研究的目的是研究与凝血酶刺激时间相关的血小板功能的一些变化。测试显示,在头三天,BTG水平的释放增加,同时出现血小板“耗竭”,这表现为血小板生成MDA减少,随后转变为高活性状态,在第10至15天MDA产生量达到最大。