ALCOHOL, ALCOHOLISM AND PLATELETS

酒精和酒精中毒对血小板的影响是值得关注的， 由于酒精对心血管疾病发病率的潜在影响 涉及血小板的疾病，包括血栓和出血性 中风、动脉粥样硬化和心肌梗塞。流行的观点是 虽然滥用是有害的，但适度消费可能是有害的 有益的，但这并没有很好的记录。酒精和酒精的影响 饮酒对血小板功能的影响 注意，结果好坏参半。一般而言，血小板功能受到抑制。 当饮酒或在体外添加酒精时，血小板聚集 用常规比浊法测定富血小板血浆中的浓度 或者洗过的血小板。其他研究表明，在这些患者中，血小板被激活 然而，酒精制剂。这一领域的两个缺点 研究一直缺乏对酒精对人的影响的系统研究 使用一致的技术和缺乏生理学的血小板 为研究血小板功能做准备。出于这些原因，我们 利用全血血小板进行了初步研究 聚合技术，它允许在 血小板、其他形成的元素和血浆成分。这些研究 根据饮酒方式的不同，显示出显著不同的结果 曝光。在体外酒精，在生理上可以达到的水平，产生 诱导ADP释放对大鼠或人血中血小板聚集的影响 红细胞，然后激活钙依赖的血小板 举止。有限的初步实验表明，慢性、低剂量的 酒精对大鼠的活体暴露，类似于轻度中毒和 酒精依赖，可能抑制胶原诱导的聚集。这个 假设酒精对血小板的影响是由其他因素调节的。 血液中形成的元素，并取决于剂量和持续时间 曝光。具体目标是确定急性和慢性疾病的影响。 酒精对大鼠血小板功能参数和出血时间的影响 全血；确定环境酒精水平的作用，而不是 暴露史，对血小板功能和出血时间的影响； 评价红细胞-血小板相互作用对血小板的影响 酒精的功能影响；以及评估其他物质的潜在作用 形成元素对酒精对血小板的影响。这些研究将是 在急性和慢性酒精消费大鼠模型上通过 吸入，这会导致可预测的血液酒精水平，使用 体外全血血小板聚集技术。体外研究将 也是在人血中进行的。

Effects of alcohol and alcoholism on blood platelets are of interest, owing to potential effects of alcohol on the incidence of cardiovascular disorders involving platelets, including thrombotic and hemorrhagic stroke, atherosclerosis, and myocardial infarction. The popular view is that although abuse is detrimental, moderate consumption might be beneficial, but this is not well documented. The effects of alcohol and alcohol consumption on platelet function have received substantial attention, with mixed results. In general, platelet function is inhibited when alcohol is consumed or added in vitro, and platelet aggregation is measured by conventional turbidometric techniques in platelet rich plasma or washed platelets. Other studies show platelet activation in these preparations by alcohol, however. Two shortcomings in this area of research have been the lack of systematic study of alcohol's effects on platelets using consistent techniques, and the lack of physiological preparations for the study of platelet function. For these reasons, we have conducted preliminary studies utilizing whole blood platelet aggregation techniques, which allow physiological interaction between platelets, other formed elements, and plasma constituents. These studies show remarkably different results depending on the mode of alcohol exposure. In vitro alcohol, at physiologically attainable levels, produces platelet aggregation in rat or human blood by inducing release of ADP from red blood cells, which then activates platelets in a Ca++ dependent manner. Limited preliminary experiments suggest that chronic, low dose in vivo exposure of rats to alcohol, analogous to mild intoxication and alcohol dependence, might inhibit aggregation induced by collagen. The hypothesis is that effects of alcohol on platelets are modulated by other formed elements in blood, and are dependent on dose and duration of exposure. The specific aims are to determine effects of acute and chronic alcohol in rats on platelet functional parameters and bleeding time in whole blood; to determine the role of ambient alcohol level, as opposed to exposure history, on platelet function and bleeding time; to critically evaluate the role of erythrocyte-platelet interactions on platelet functional effects of alcohol; and to evaluate the potential role of other formed elements on platelet effects of alcohol. These studies will be performed in rat models of acute and chronic alcohol consumption via inhalation, which results in a predictable level of blood alcohol, using ex vivo whole blood platelet aggregation techniques. In vitro studies will also be performed in human blood.