Barzó P, Marmarou A, Fatouros P, Corwin F, Dunbar J
Division of Neurosurgery, Medical College of Virginia, Richmond 23298, USA.
J Neurosurg. 1996 Dec;85(6):1113-21. doi: 10.3171/jns.1996.85.6.1113.
The authors posit that cellular edema is the major contributor to brain swelling in diffuse head injury and that the contribution of vasogenic edema may be overemphasized. The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury and to what extent barrier permeability is affected by the secondary insults of hypoxia and hypotension. The BBB disruption was quantified and visualized using T1-weighted magnetic resonance (MR) imaging following intravenous administration of the MR contrast agent gadolinium-diethylenetriamine pentaacetic acid. To avoid the effect of blood volume changes, the maximum signal intensity (SI) enhancement was used to calculate the difference in BBB disruption. A new impact-acceleration model was used to induce closed head injury. Forty-five adult Sprague-Dawley rats were separated into four groups: Group I, sham operated (four animals), Group II, hypoxia and hypotension (four animals), Group III, trauma only (23 animals), and Group IV, trauma coupled with hypoxia and hypotension (14 animals). After trauma was induced, a 30-minute insult of hypoxia (PaO2 40 mm Hg) and hypotension (mean arterial blood pressure 30 mm Hg) was imposed, after which the animals were resuscitated. In the trauma-induced animals, the SI increased dramatically immediately after impact. By 15 minutes permeability decreased exponentially and by 30 minutes it was equal to that of control animals. When trauma was coupled with secondary insult, the SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically on reperfusion and was equal to that of control by 60 minutes after the combined insult. In conclusion, the authors suggest that closed head injury is associated with a rapid and transient BBB opening that begins at the time of the trauma and lasts no more than 30 minutes. It has also been shown that addition of posttraumatic secondary insult-hypoxia and hypotension-prolongs the time of BBB breakdown after closed head injury. The authors further conclude that MR imaging is an excellent technique to follow (time resolution 1-1.5 minutes) the evolution of trauma-induced BBB damage noninvasively from as early as a few minutes up to hours or even longer after the trauma occurs.
作者认为细胞性水肿是弥漫性头部损伤中脑肿胀的主要原因,而血管源性水肿的作用可能被过度强调了。本研究的目的是确定弥漫性闭合性头部损伤中血脑屏障(BBB)变化的早期时间进程,以及缺氧和低血压等继发性损伤对屏障通透性的影响程度。静脉注射磁共振(MR)造影剂钆-二乙烯三胺五乙酸后,采用T1加权磁共振成像对血脑屏障破坏进行定量和可视化。为避免血容量变化的影响,使用最大信号强度(SI)增强来计算血脑屏障破坏的差异。采用一种新的撞击-加速模型诱导闭合性头部损伤。45只成年Sprague-Dawley大鼠分为四组:第一组,假手术组(4只动物);第二组,缺氧和低血压组(4只动物);第三组,仅创伤组(23只动物);第四组,创伤合并缺氧和低血压组(14只动物)。诱导创伤后,施加30分钟的缺氧(动脉血氧分压40 mmHg)和低血压(平均动脉血压30 mmHg)刺激,然后对动物进行复苏。在创伤诱导的动物中,撞击后SI立即显著增加。到15分钟时通透性呈指数下降,到30分钟时与对照动物相等。当创伤合并继发性损伤时,创伤后SI增强较低,这与血压和血流降低一致。然而,再灌注时SI显著增加,联合损伤后60分钟时与对照相等。总之,作者认为闭合性头部损伤与创伤时开始且持续不超过30分钟的快速且短暂的血脑屏障开放有关。还表明创伤后继发性损伤(缺氧和低血压)的叠加会延长闭合性头部损伤后血脑屏障破坏的时间。作者进一步得出结论,磁共振成像(时间分辨率为1 - 1.5分钟)是一种极好的技术,可在创伤发生后几分钟至数小时甚至更长时间内无创地跟踪创伤诱导的血脑屏障损伤的演变。