A Plasmatic Factor May Cause Platelet Activation in Acute Ischemic Stroke
作者:
Rajiv Joseph,
K. Welch,
S. Oster,
S. Grunfeld,
G. D'Andrea,
期刊:
Circulation Research
(OVID Available online 1989)
卷期:
Volume 65,
issue 6
页码: 1679-1687
ISSN:0009-7330
年代: 1989
出版商: OVID
关键词: cerebrovascular diseases;platelets;calcium;collagen;thiombin;platelet activating factor
数据来源: OVID
摘要:
To study the pathogenesis of platelet activation in ischemic stroke, ionized calcium ([Cai2+]) was measured in aequorin-loaded gel-filtered platelets in the basal and stimulated state. Basal [Cai2+] was increased in stroke patients maximally 36-72 hours after onset. The increase in [Cai2+] after stimulation with thrombin, collagen, and platelet-activating factor were also greater in stroke patients, but the profiles of these [Cai2+] changes were parallel to control. Cross incubation of control platelets with plasma from stroke patients resulted in raised basal [Cai2+] and caused the release of serotonin from platelets. These results indicate that the higher platelet basal [Cai2+] 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.
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