抄録
When human platelets in plasma were exposed to a small amount (nonaggregating concentration) of collagen, epinephrine or arachidonic acid, their responsiveness to aggregating agents were potentiated and they were aggregated by a subsequent addition of nonaggregating concentration of the stimulants. Otherwise the nonaggregating concentrations of the stimulants were uncapable to induce platelet aggregation. The potentiation of platelet responsiveness to aggregating agents was also caused by collagen- or epinephrine-treated platelet menbranes, but not by arachidonic acid-treated membranes. Furthermore, the soluble fraction of collagen- or epinephrine-treated membranes contained some material responsible for platelet potentiation, indicating that the responsible material was released from platelet membranes by collagen or epinephrine. It is suggested that the material may be arachidonic acid since the soluble fraction of collage- or epinephrine-treated membranes contained a larger amount of the precursor of prostaglandin F2α than the untreated membranes and arachidonic acid is the precursor of Prostaglandin F2α. The potentiation of platelet aggregability by the small amounts of the stimulants was increased in nephrotic syndrome whose albumin concentration in plasma is low, and the increased potentiation was abolished by the addition of albumin. The abolishment of the potentiation of platelets by albumin could be explained by postulating that some part of arachidonic acid released from membranes immediately binds to albumin and becomes unavailable to platelets.
