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DYSREGULATION OF Ca2+ MOVEMENT IN PLATELETS FROM PATIENTS WITH ACUTE ISCHAEMIC STROKE

1 Platelets play a pivotal role during acute ischaemic stroke. An increase in cytosolic Ca2+ concentrations ([Ca2+]i) triggers intracellular signal transduction, leading to platelet aggregation and thrombosis. In the present study, we examined the differences between platelets from acute ischaemic stroke patients and at‐risk controls in terms of the increase in platelet [Ca2+]i. 2 Thirty‐one patients with acute ischaemic stroke and 27 at‐risk controls were enrolled in the present study. Platelet [Ca2+]i was measured using the fluorescent dye fura‐2 after stimulation with 100 µmol/L arachidonic acid (AA), 10 µmol/L ADP, 1 µmol/L platelet‐activation factor (PAF) and 0.1 U/mL thrombin. 3 Basal [Ca2+]i was higher in the stroke group compared with at‐risk controls, irrespective of the presence or absence of extracellular Ca2+. In Ca2+‐containing medium, both PAF and ADP, but not AA and thrombin, significantly increased platelet [Ca2+]i in the stroke group compared with the at‐risk controls. However, in Ca2+‐free medium, only PAF significantly increased platelet [Ca2+]i in the stroke group compared with the at‐risk controls. Basal [Ca2+]i and PAF‐induced platelet [Ca2+]i increases were still higher in the stroke group at the subacute stage than in the at‐risk controls. 4 The results of the present study provide direct evidence that Ca2+ signalling in platelets from acute ischaemic stroke patients was altered in response to particular stimuli. The dysregulation of Ca2+ movement in platelets may persist up to the subacute stage of ischaemic stroke.