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血浆高黏滞度在皮质下动脉硬化性脑病(宾斯旺格病)中的作用。

The role of plasma hyperviscosity in subcortical arteriosclerotic encephalopathy (Binswanger's disease).

作者信息

Schneider R, Ringelstein E B, Zeumer H, Kiesewetter H, Jung F

出版信息

J Neurol. 1987 Feb;234(2):67-73. doi: 10.1007/BF00314104.

Abstract

Five haemorheological variables (haematocrit, plasma viscosity, red cell aggregation, red cell deformability and yield shear stress) and the plasma fibrinogen concentration were determined in blood samples from 21 untreated patients with subcortical arteriosclerotic encephalopathy (SAE, Binswanger's disease). The results were compared with those obtained in blood samples from 40 untreated patients with lacunar infarcts and from 275 healthy control subjects without vascular risk factors. Pathological ("solid body") flow behaviour was detected in the blood of both groups of patients (SAE and lacunar infarcts). However, highly elevated plasma viscosity was a consistent feature only of SAE. The authors present the hypothesis that the high plasma viscosity in patients with SAE may account for the progressive degeneration of cerebral white matter. It is postulated that microcirculatory abnormalities due to microrheological changes may be one of the many missing links in the pathophysiology of SAE.

摘要

对21例未经治疗的皮质下动脉硬化性脑病(SAE,宾斯旺格病)患者的血样测定了五项血液流变学指标(血细胞比容、血浆粘度、红细胞聚集性、红细胞变形性和屈服切应力)以及血浆纤维蛋白原浓度。将结果与40例未经治疗的腔隙性脑梗死患者和275例无血管危险因素的健康对照者的血样结果进行了比较。在两组患者(SAE和腔隙性脑梗死)的血液中均检测到病理性(“固体样”)流动行为。然而,血浆粘度高度升高仅是SAE的一个一致特征。作者提出假说,SAE患者的高血浆粘度可能是脑白质进行性退变的原因。据推测,由于微观流变学变化导致的微循环异常可能是SAE病理生理学中众多缺失环节之一。

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