The effects of aspirin and hypothermia on platelet function in vivo
The effects of aspirin and hypothermia on platelet function in vivo
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DOI：
10.1046/j.1365-2141.1999.01146.x
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发表时间：
1999-01-01
影响因子：
6.5
通讯作者：
Valeri, CR
中科院分区：
文献类型：
--
作者：
Michelson, AD;Barnard, MR;Valeri, CR
接受低温心肺转流术的患者经常接受阿司匹林治疗。低温、阿司匹林和心肺转流术均能诱导血小板功能缺陷，但阿司匹林和低温在这方面的作用是否相加尚不清楚。为了在人体内解决这个问题，健康志愿者的前臂皮肤温度在摄入650 mg阿司匹林之前和之后16小时平衡并保持在正常体温（32 ° C）或低温（28 ° C或22 ° C）。在前臂上进行标准化的模板出血时间，并通过全血流动细胞术（反映颗粒分泌）和放射免疫测定法测定从伤口流出的血液中血小板表面P-选择素的表达（血栓素A（2）的稳定代谢物）。低温导致出血时间显著延长。在常温下，阿司匹林可延长出血时间，但仅轻微增加低温引起的出血时间延长。低温可消除血小板表面P选择素的上调。在常温或低温条件下，阿司匹林对血小板表面P-选择素的最大表达没有影响。低温和阿司匹林均导致血液中血栓素B-2明显减少。虽然阿司匹林轻微增加了低体温诱导的血液中血栓素B-2的减少，但在不存在阿司匹林的情况下，在低温条件下血液中产生的血栓素浓度对血小板表面P-选择素或全血中的血小板聚集没有影响。总之，由标准化出血时间伤口流出的血液的三个独立参数（出血时间、血小板表面P-选择素和血栓素B-2）确定，阿司匹林在体内没有显著增加低血糖诱导的血小板功能障碍。
Patients undergoing hypothermic cardiopulmonary bypass are often receiving aspirin therapy. Hypothermia, aspirin and cardiopulmonary bypass can each induce a platelet function defect, but it is not known if the effects of aspirin and hypothermia are additive in this regard. To address this question in humans in vivo, the forearm skin temperature of healthy volunteers was equilibrated and maintained at either normothermia (32 degrees C) or hypothermia (28 degrees C or 22 degrees C) before and 16 h after the ingestion of 650 mg aspirin. A standardized template bleeding time was performed on the forearm and the shed blood emerging from the wound was assayed for platelet surface P-selectin expression by whole blood now cytometry (reflecting of granule secretion) and thromboxane B-2 (the stable metabolite of thromboxane A(2)) by radioimmunoassay Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time under normothermic conditions, but only minimally augmented the hypothermia-induced prolongation of the bleeding time, Platelet surface P-selectin up-regulation in shed blood was abolished by hypothermia. Aspirin had no effect on maximal platelet surface P-selectin expression under normothermic or hypothermic conditions. Both hypothermia and aspirin resulted in markedly reduced shed blood thromboxane B-2. Although aspirin slightly augmented the hypothermia-induced reduction in shed blood thromboxane B-2, the concentration of thromboxane generated in shed blood under hypothermic conditions in the absence of aspirin had no effect on platelet surface P-selectin or platelet aggregation in whole blood. In conclusion, as determined by three independent parameters of the shed blood emerging from a standardized bleeding time wound (bleeding time, platelet surface P-selectin, and thromboxane B-2), aspirin did not significantly augment hypothermia-induced platelet dysfunction in vivo.