Gentry P A, Tremblay R R, Ross M L
Department of Biomedical Studies, Ontario Veterinary College, Guelph, Ontario.
Am J Vet Res. 1989 Jun;50(6):919-22.
The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.
评估了阿司匹林对牛血小板功能以及对受刺激血小板中血栓素A2（TXA2）生成的影响。给荷斯坦奶牛口服单剂量阿司匹林（100毫克/千克体重），并在治疗前及治疗后7天定期采集血样。通过使用特定的放射免疫分析法测量稳定代谢产物血栓素B2来评估TXA2的生成。在服用阿司匹林后4小时内，无论使用胶原蛋白、二磷酸腺苷还是血小板活化因子引发血小板聚集，TXA2的生成均显著（P小于0.05）减少。尽管受刺激血小板释放TXA2受到抑制，但通过聚集初始速率和聚集程度评估的血小板功能并未受阿司匹林给药的影响。对胶原蛋白、二磷酸腺苷或血小板活化因子的聚集程度与阿司匹林治疗前后血小板释放的TXA2量无关。结果表明，TXA2的形成不是受刺激牛血小板聚集所涉及的主要生化途径。
