Effects of Aspirin and Hypothermia on Platelet Function in Vivo

摘要

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 deg C) or hypothermia (28 deg C or 22 deg C) before and 16 hours after the ingestion of aspirin 650 mg. Hypothermia was achieved by a stream of air cooled by dry ice or placing the volunteer in a 4 deg C walk-in cold room. Skin temperature was monitored by a surface thermometer. A standardized template bleeding time was performed on the forearm and the shed blood emerging from the wound was assayed for: (a) platelet surface P-selectin-expression by whole blood flow cytometry (reflecting a granule secretion), (b) total shed blood hemoglobin and shed blood volume (reflecting blood loss), and (c) thromboxane B sub 2 (the stable metabolite of thromboxane A sub 2) by radioimmunoassay. Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time under normothermic conditions, but did not augment 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. Aspirin did not augment hypothermia-induced blood loss, as determined by total shed blood hemoglobin and shed blood volume. Both hypothermia and aspirin resulted in markedly reduced shed blood thromboxane B sub 2.