Iwamoto T, Kubo H, Takasaki M
Department of Geriatric Medicine, Tokyo Medical College Hospital.
Stroke. 1995 Jan;26(1):52-6. doi: 10.1161/01.str.26.1.52.
The sites of platelet activation in ischemic stroke are still unclear because previous reports have not identified them and various factors accompanied by stroke can activate platelets. We therefore examined the sites of platelet activation in patients with various types of ischemic stroke.
The ratio of the plasma concentration of beta-thromboglobulin (BTG) in the internal jugular vein to that in the antecubital vein (BTG-B) was calculated as an indicator of platelet activation in the cerebral circulation. Plasma BTG concentration was determined in 75 control subjects and in 186 patients with various subtypes of ischemic stroke including lacunar, atherothrombotic, and cardioembolic strokes, transient ischemic attacks, and Binswanger's disease. The BTG ratio was evaluated with regard to subtype of stroke, time of blood sampling, size of infarct, presence of vascular lesions, and the effect of ticlopidine administration.
The mean BTG ratio was increased even in the chronic phase of most subtypes of stroke with the exception of cardioembolic stroke, which exhibited a persistent elevation of BTG-B concentrations. Patients with Binswanger's disease showed a significant (P < .01) and frequent elevation of BTG ratio. High BTG ratios occurred in cases with vascular lesions observed on cerebral angiography. There was no correlation between the BTG ratio and infarct size. Use of ticlopidine was partially associated with a lower BTG ratio.
Platelets were activated in the cerebral circulation of patients with stroke even in the chronic phase, which suggests the development of underlying vascular lesions and of thrombogenesis with or without infarction. Platelets were activated mainly within the heart in cases of cardioembolic stroke. An enhanced release reaction secondary to platelet activation was often seen in patients with Binswanger's disease, which indicates that its pathophysiology differs from that of other subtypes of stroke.
缺血性卒中时血小板激活的部位仍不清楚，因为既往报告未明确这些部位，且卒中伴随的多种因素可激活血小板。因此，我们研究了各类缺血性卒中患者血小板激活的部位。
计算颈内静脉血浆β-血小板球蛋白（BTG）浓度与肘前静脉血浆BTG浓度的比值（BTG-B），作为脑循环中血小板激活的指标。测定了75名对照者以及186例各类缺血性卒中亚型患者（包括腔隙性、动脉粥样硬化血栓形成性和心源性栓塞性卒中、短暂性脑缺血发作以及宾斯旺格病）的血浆BTG浓度。根据卒中亚型、采血时间、梗死灶大小、血管病变情况以及噻氯匹定给药的影响评估BTG比值。
除心源性栓塞性卒中（其BTG-B浓度持续升高）外，大多数卒中亚型即使在慢性期平均BTG比值也升高。宾斯旺格病患者的BTG比值显著升高（P <.01）且频繁出现。脑血管造影显示有血管病变的病例中BTG比值较高。BTG比值与梗死灶大小无相关性。使用噻氯匹定与较低的BTG比值部分相关。
即使在慢性期，卒中患者的脑循环中血小板也被激活，这提示潜在血管病变以及有或无梗死的血栓形成过程的发展。心源性栓塞性卒中时血小板主要在心脏内被激活。宾斯旺格病患者常可见继发于血小板激活的增强释放反应，这表明其病理生理学与其他卒中亚型不同。
