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Address correspondence to Soo Hwan Pai, M.D., Department of Clinical Pathology, Inha University Hospital, 7-206, 3-ga, Shinheung-dong, Jung-gu, Inchon 400-103, Republic of Korea; tel 82 32 890 2502; fax 82 32 890 2529; e-mail shpaimd{at}inha.ac.kr.
To investigate the effects of storage temperature on the responsiveness to agonists of human platelets prepared from stored blood, we measured the aggregability and acid-base status of platelets from 96 healthy subjects before and after storage of whole blood at 4°C and room temperature (RT) up to 48 hr. After 24 hr storage at 4°C, there were no significant differences in agonist-induced platelet aggregability, compared to fresh specimens. When blood was kept at RT for 24 hr, all of the platelet samples showed non-responsiveness (< 20% aggregability) to epinephrine and 70% (67/96) revealed impaired responsiveness (20 to 60% aggregability) to adenosine diphosphate (ADP); there were no samples that showed impaired-or non-responsiveness to collagen or ristocetin. Among the 67 samples that showed impaired responsiveness to ADP after RT storage, 62 (93%) exhibited the loss of a secondary wave of aggregation in response to ADP. After storage of blood at RT for 48 hr (pH 6.81 ± 0.06), mean values of maximal platelet aggregability to epinephrine, ADP, collagen, and ristocetin were 8%, 16%, 19%, and 70%, which were significantly lower than the corresponding mean values after storage of blood at 4°C for 48 hr (pH 7.04 ± 0.04) (ie, 66%, 69%, 102%, and 91%, p <0.01). In summary, refrigerated storage of human blood improves the stability of platelet responsiveness to agonists. Storage at RT causes platelet non-responsiveness to epinephrine and disturbs the release reaction of endogenous ADP.
Keywords: platelet aggregability, blood storage, epinephrine, ADP, collagen, ristocetin
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