Rand M L, Packham M A, Kinlough-Rathbone R L, Fraser Mustard J
Department of Biochemistry, University of Toronto, Canada.
Thromb Haemost. 1988 Jun 16;59(3):383-7.
Ethanol, at physiologically tolerable concentrations, did not affect the primary phase of ADP-induced aggregation of human or rabbit platelets, which is not associated with the secretion of granule contents. Potentiation by epinephrine of the primary phase of ADP-induced aggregation of rabbit platelets was also not inhibited by ethanol. However, ethanol did inhibit the secondary phase of ADP-induced aggregation which occurs with human platelets in citrated platelet-rich plasma and is dependent on the formation of thromboxane A2. Inhibition by ethanol of thromboxane production by stimulated platelets is likely due to inhibition of the mobilization of arachidonic acid from membrane phospholipids, as ethanol had little or no effect on aggregation and secretion induced by arachidonic acid or the thromboxane mimetic U46619. Rabbit platelet aggregation and secretion in response to low concentrations of collagen, thrombin, or PAF were inhibited by ethanol. Inhibition of the effects of thrombin and PAF was also observed with aspirin-treated platelets. Thus, in addition to inhibiting the mobilization of arachidonate for thromboxane formation that occurs with most agonists, ethanol can also inhibit aggregation and secretion through other effects on platelet responses.
在生理可耐受浓度下，乙醇不影响人或兔血小板由二磷酸腺苷（ADP）诱导的初级聚集阶段，该阶段与颗粒内容物的分泌无关。乙醇也不抑制肾上腺素对兔血小板由ADP诱导的初级聚集阶段的增强作用。然而，乙醇确实抑制了在富含血小板的枸橼酸盐血浆中由人血小板发生的、依赖于血栓素A2形成的ADP诱导的次级聚集阶段。乙醇对受刺激血小板产生血栓素的抑制作用可能是由于抑制了花生四烯酸从膜磷脂的动员，因为乙醇对花生四烯酸或血栓素类似物U46619诱导的聚集和分泌几乎没有影响。乙醇抑制了兔血小板对低浓度胶原、凝血酶或血小板活化因子（PAF）的聚集和分泌。在用阿司匹林处理的血小板中也观察到了对凝血酶和PAF作用的抑制。因此，除了抑制大多数激动剂作用下发生的花生四烯酸向血栓素形成的动员外，乙醇还可通过对血小板反应的其他作用来抑制聚集和分泌。
