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纤维蛋白原、血液黏度与脑缺血

Fibrinogen, blood viscosity, and cerebral ischemia.

作者信息

Grotta J, Ostrow P, Fraifeld E, Hartman D, Gary H

出版信息

Stroke. 1985 Mar-Apr;16(2):192-8. doi: 10.1161/01.str.16.2.192.

Abstract

This study examines the effect of fibrinogen and consequent blood viscosity reduction on cerebral blood flow and cellular injury following severe cerebral ischemia for 30 minutes in 78 Wistar rats. In half of these rats 10 to 15 cc's of blood was removed and replaced with a mixture of 5% albumin and autologous red blood cells maintaining a constant hematocrit but resulting in a 30% decrease in fibrinogen and corresponding reduction in viscosity. Fibrinogen reduction in a slight increase in baseline CBF and the elimination of post-ischemic hyperemia at 24 hours. Both study and control animals showed a similar decrease in CBF at 30 minutes and 2 hours. There was no significant difference in the severity of ischemic cellular change between the fibrinogen reduction group and controls, although there was a significant inverse relationship between the amount of viscosity change and severity of cellular injury within the treatment group. Fibrinogen reduction alone cannot significantly ameliorate ischemic injury in this model. Viscosity reduction therapy should include reduction of hematocrit and alteration of red cell deformability.

摘要

本研究在78只Wistar大鼠中,考察了严重脑缺血30分钟后纤维蛋白原及随之而来的血液粘度降低对脑血流量和细胞损伤的影响。在其中一半的大鼠中,抽取10至15毫升血液,并用5%白蛋白和自体红细胞的混合物进行置换,维持血细胞比容恒定,但纤维蛋白原降低30%,粘度相应降低。纤维蛋白原降低使基线脑血流量略有增加,并消除了24小时后的缺血后充血。研究组和对照组动物在30分钟和2小时时脑血流量均有相似程度的下降。纤维蛋白原降低组与对照组之间缺血性细胞变化的严重程度无显著差异,尽管在治疗组内粘度变化量与细胞损伤严重程度之间存在显著的负相关。在该模型中,单纯降低纤维蛋白原并不能显著改善缺血性损伤。降低粘度的治疗应包括降低血细胞比容和改变红细胞变形能力。

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