Abstract
Objective—To compare the interaction of endogenous ADP with collagen and thromboxane A2 (TXA2) during collagen-induced platelet aggregation between platelets from healthy cattle and those with Chediak-Higashi syndrome (CHS).
Population Sample—Platelets harvested from blood samples from healthy Japanese Black cattle and those with CHS.
Procedures—Aggregation of gel-filtered platelets; release of ATP-ADP; and generation of thromboxane B2 (TXB2), a metabolite of TXA2, were measured.
Results—The potency of collagen to induce aggregation in platelets of cattle with CHS (ie, CHS platelets) was less than a tenth of that in platelets of healthy cattle (ie, control platelets). Platelet aggregation induced by collagen at an intermediate concentration depended on the coexistence of ADP and TXA2, suggesting that released ADP cannot cause platelet aggregation by itself. Collagen-induced ADP release was markedly decreased, whereas TXB2 production was slightly low in CHS platelets, compared with that in control platelets. A combination of subthreshold amounts of ADP and 9,11-dideoxy-9α, 11α-methano-epoxy-prostaglandin F2α (U46619), a TXA2 analogue, caused platelet aggregation. Similarly, a combination of subthreshold amounts of collagen and ADP caused platelet aggregation, whereas collagen and U46619 were not synergistic.
Conclusions and Clinical Relevance—Deficient ADP release ensuing from the δ-storage pool deficiency in platelets from cattle with CHS resulted in reduction of collagen-induced platelet aggregation, through attenuation of synergism between TXA2 and ADP and between ADP and collagen. Furthermore, results of the study reported here indicated that TXA2 was important for aggregation of bovine platelets.
