血栓素A2作为血小板活化因子诱导人血小板聚集介质的作用。

Role of thromboxane A2 as a mediator of platelet-activating-factor-induced aggregation of human platelets.

McCulloch R K, Summers J, Vandongen R, Rouse I L

Department of Medicine, University of Western Australia, Royal Perth Hospital.

Clin Sci (Lond). 1989 Jul;77(1):99-103. doi: 10.1042/cs0770099.

Abstract

At present it is unclear whether platelet-activating-factor (PAF)-induced aggregation is mediated by thromboxane. To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen. 2. Collagen and PAF induced aggregation and secretion in human platelets in a dose-related manner. 3. Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen. 4. Aspirin strongly inhibited the aggregation rate of collagen-induced platelet aggregation, but had no measurable effect on the rate of PAF-induced aggregation. 5. Inconsistencies reported in previous studies of the effect of aspirin on PAF-induced platelet aggregation may be explained, in part, by the doses of PAF used and the method of inactivating cyclo-oxygenase (in vitro compared with in vivo). 6. Our results suggest that the initial events of PAF-induced aggregation are independent of thromboxane A2 formation and that thromboxane A2 plays only a minor role in the later phase of PAF-induced aggregation.

摘要

目前尚不清楚血小板活化因子（PAF）诱导的聚集是否由血栓素介导。为了获取有关此事件的更多信息，我们比较了阿司匹林对PAF和胶原诱导的血小板聚集及分泌的影响。2. 胶原和PAF以剂量相关的方式诱导人血小板聚集和分泌。3. 阿司匹林抑制了PAF和胶原诱导的血小板聚集及分泌的程度，但对胶原的抑制程度要大得多。4. 阿司匹林强烈抑制胶原诱导的血小板聚集速率，但对PAF诱导的聚集速率没有可测量的影响。5. 先前关于阿司匹林对PAF诱导的血小板聚集作用的研究中所报告的不一致性，部分可能是由于所用PAF的剂量以及环氧化酶失活的方法（体外与体内相比）所致。6. 我们的结果表明，PAF诱导聚集的初始事件独立于血栓素A2的形成，并且血栓素A2在PAF诱导聚集的后期仅起次要作用。