水肿形成过程中的血脑屏障水通透性和脑渗透压物质含量

Blood-brain barrier water permeability and brain osmolyte content during edema development.

作者信息

Olson J E, Banks M, Dimlich R V, Evers J

机构信息

Wright State University, School of Medicine, Department of Emergency Medicine, Cox Institute, Kettering, OH 45429, USA.

出版信息

Acad Emerg Med. 1997 Jul;4(7):662-73. doi: 10.1111/j.1553-2712.1997.tb03757.x.

DOI:10.1111/j.1553-2712.1997.tb03757.x

PMID:9223688

Abstract

OBJECTIVE

To determine mechanisms that limit changes in brain water content during acute edema development.

METHODS

A controlled, laboratory investigation of the physiologic and biochemical correlates of osmotic edema was performed in rats. Hypoosmotic hyponatremia was induced by intraperitoneal injection of distilled water. Serum osmolality and electrolytes and regional blood-brain barrier water permeability. Surface area (P.S) product, osmolyte contents, and capillary size were determined during 120 minutes of hypoosmotic brain edema development. Cerebral water content predicted from these data using a mathematical model of brain water movements was compared with measured changes in brain water content.

RESULTS

Fifteen minutes after distilled water injection, mean +/- SEM blood serum osmolality and sodium concentration decreased from 291 +/- 3 mOsm and 131 +/- 13 mmol/L to 267 +/- 3 mOsm and 102 +/- 9 mmol/L, respectively. Specific gravity of cerebral gray matter, cerebral white matter, and basal ganglia decreased throughout the hypoosmotic exposure period and, for gray and white matter, correlated with blood serum osmolality and sodium plus potassium content. Glutamate, but not glutamine, glycine, or taurine, decreased 120 minutes after water injection. The regional water P.S product decreased by 40% to 60% within 60 minutes of the water injection, while capillary diameters in gray and white matter were unchanged. Brain water movements calculated from the mathematical model correctly predicted actual brain water content only if the hydraulic conductivity of the blood-brain barrier was allowed to vary in proportion to the measured P.S product and the measured loss of brain osmolytes was incorporated into the formulation.

CONCLUSIONS

During the first hours of hypoosmotic hyponatremia, changes in brain volume are limited by increased resistance to osmotic flux of water into the brain and reduction in the brain content of inorganic and, to a smaller degree, organic osmolytes.

摘要

目的

确定在急性水肿发展过程中限制脑含水量变化的机制。

方法

在大鼠身上进行了一项关于渗透性水肿的生理和生化相关性的对照实验室研究。通过腹腔注射蒸馏水诱导低渗性低钠血症。在低渗性脑水肿发展的120分钟内，测定血清渗透压、电解质以及区域血脑屏障水通透性、表面积（P.S）乘积、渗透溶质含量和毛细血管大小。使用脑水运动数学模型根据这些数据预测的脑含水量与实测的脑含水量变化进行比较。

结果

注射蒸馏水15分钟后，平均±标准误血清渗透压和钠浓度分别从291±3 mOsm和131±13 mmol/L降至267±3 mOsm和102±9 mmol/L。在整个低渗暴露期，脑灰质、脑白质和基底神经节的比重均下降，对于灰质和白质，其与血清渗透压以及钠加钾含量相关。注射水120分钟后，谷氨酸含量下降，但谷氨酰胺、甘氨酸或牛磺酸含量未下降。注水后60分钟内，区域水P.S乘积下降了40%至60%，而灰质和白质中的毛细血管直径未变。只有当血脑屏障的水力传导率与实测的P.S乘积成比例变化且将实测的脑渗透溶质损失纳入公式时，根据数学模型计算的脑水运动才能正确预测实际脑含水量。