The effects of aspirin and hypothermia on platelet function in vivo

Patients undergoing hypothermic cardiopulmonary bypass are often receiving aspirin therapy. Hypothermia, aspirin and cardiopulmonary bypass can each i nduce a platelet function defect, but it is not known if the effects of asp irin and hypothermia are additive in this regard. To address this question in humans in vivo, the forearm skin temperature of healthy volunteers was e quilibrated and maintained at either normothermia (32 degrees C) or hypothe rmia (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 oi granule secretion) and thromboxane B-2 (the stable metabolite of thromboxan e A(2)) by radioimmunoassay Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time un der normothermic conditions, but only minimally augmented the hypothermia-i nduced prolongation of the bleeding time, Platelet surface P-selectin up-re gulation in shed blood was abolished by hypothermia. Aspirin had no effect on maximal platelet surface P-selectin expression under normothermic or hyp othermic conditions. Both hypothermia and aspirin resulted in markedly redu ced shed blood thromboxane B-2. Although aspirin slightly augmented the hyp othermia-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 platele t aggregation in whole blood. In conclusion, as determined by three indepen dent parameters of the shed blood emerging from a standardized bleeding tim e wound (bleeding time, platelet surface P-selectin, and thromboxane B-2), aspirin did not significantly augment hypothermia-induced platelet dysfunct ion in vivo.