A plasmatic factor may cause platelet activation in acute ischemic stroke

Abstract

To study the pathogenesis of platelet activation in ischemic stroke, ionized calcium ([Ca(i)2+]) was measured in aequorin-loaded gel-filtered platelets in the basal and stimulated state. Basal [Ca(i)2+] was increased in stroke patients maximally 36-72 hours after onset. The increase in [Ca(i)2+] after stimulation with thrombin, collagen, and platelet-activating factor were also greater in stroke patients, but the profiles of these [Ca(i)2+] changes were parallel to control. Cross incubation of control platelets with plasma from stroke patients resulted in raised basal [Ca(i)2+] and caused the release of serotonin from platelets. These results indicate that the higher platelet basal [Ca(i)2+] in stroke patients represents a lowered threshold for activation and that this may be due to a plasmatic factor rather than a primary platelet defect.