title: Dysregulation of Ca2+ movement in platelets from patients with acute ischaemic stroke.
abstract: 1. Platelets play a pivotal role during acute ischaemic stroke. An increase in cytosolic Ca(2+) concentrations ([Ca(2+)](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 [Ca(2+)](i). 2. Thirty-one patients with acute ischaemic stroke and 27 at-risk controls were enrolled in the present study. Platelet [Ca(2+)](i) was measured using the fluorescent dye fura-2 after stimulation with 100 micromol/L arachidonic acid (AA), 10 micromol/L ADP, 1 micromol/L platelet-activation factor (PAF) and 0.1 U/mL thrombin. 3. Basal [Ca(2+)](i) was higher in the stroke group compared with at-risk controls, irrespective of the presence or absence of extracellular Ca(2+). In Ca(2+)-containing medium, both PAF and ADP, but not AA and thrombin, significantly increased platelet [Ca(2+)](i) in the stroke group compared with the at-risk controls. However, in Ca(2+)-free medium, only PAF significantly increased platelet [Ca(2+)](i) in the stroke group compared with the at-risk controls. Basal [Ca(2+)](i) and PAF-induced platelet [Ca(2+)](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 Ca(2+) signalling in platelets from acute ischaemic stroke patients was altered in response to particular stimuli. The dysregulation of Ca(2+) movement in platelets may persist up to the subacute stage of ischaemic stroke.
authors.affiliation: Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
authors.forename: Nai-Wen
authors.initials: NW
authors.lastname: Tsai
authors.forename: Cheng-Hsien
authors.initials: CH
authors.lastname: Lu
authors.forename: Wen-Neng
authors.initials: WN
authors.lastname: Chang
authors.forename: Chen-Fu
authors.initials: CF
authors.lastname: Shaw
authors.forename: Chi-Ren
authors.initials: CR
authors.lastname: Huang
authors.forename: Shang-Der
authors.initials: SD
authors.lastname: Chen
authors.forename: Yao-Chung
authors.initials: YC
authors.lastname: Chuang
authors.forename: Lian-Hui
authors.initials: LH
authors.lastname: Lee
authors.forename: Chung-Ren
authors.initials: CR
authors.lastname: Jan
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000378:metabolism* / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007511:Ischemia / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology; D020521:Stroke / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D013927:Thrombosis / Q000378:metabolism / Q000473:pathology
chemical_list: D002118:Calcium