Hellal F, Bonnefont-Rousselot D, Croci N, Palmier B, Plotkine M, Marchand-Verrecchia C
UPRES EA2510, Laboratoire de Pharmacologie, Université René Descartes, 4 avenue de l'Observatoire, F-75006 Paris, France.
Neurosci Lett. 2004 Feb 26;357(1):21-4. doi: 10.1016/j.neulet.2003.12.036.
This study aims to examine the time course of the brain edema formation in relation with blood-brain barrier (BBB) disruption and cerebral hemorrhage in a murine model of diffuse brain injury. Brain water content increased at 1 h post-injury and persisted up to 7 days. This event was associated with electrolyte imbalance such as Na(+) increase within 24 h. Prominent Evans blue extravasation was also observed from 1 to 6 h post-injury. Concurrently, hemoglobin increased markedly by 1 h, reached a peak at 4 h and declined progressively within a week in association with a rise of parenchyma iron content between 24 h and 7 days. These results suggest that brain edema is vasogenic and that the hemorrhage process is involved in the BBB disruption and edema, both leading to post-traumatic secondary events.
本研究旨在探讨弥漫性脑损伤小鼠模型中脑水肿形成的时间进程及其与血脑屏障（BBB）破坏和脑出血的关系。脑含水量在损伤后1小时增加，并持续至7天。此事件与电解质失衡有关，如在24小时内钠离子增加。在损伤后1至6小时也观察到明显的伊文思蓝外渗。同时，血红蛋白在1小时时显著增加，在4小时达到峰值，并在一周内逐渐下降，同时在24小时至7天之间实质铁含量升高。这些结果表明脑水肿是血管源性的，出血过程参与了血脑屏障破坏和水肿，两者均导致创伤后继发性事件。
