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缺血性中风超急性期的水肿形成。实验室研究。

Edema formation in the hyperacute phase of ischemic stroke. Laboratory investigation.

作者信息

Gerriets Tibo, Walberer Maureen, Ritschel Nouha, Tschernatsch Marlene, Mueller Clemens, Bachmann Georg, Schoenburg Markus, Kaps Manfred, Nedelmann Max

机构信息

Department of Neurology, Justus Liebig-University Giessen, Giessen, Germany.

出版信息

J Neurosurg. 2009 Nov;111(5):1036-42. doi: 10.3171/2009.3.JNS081040.

DOI:10.3171/2009.3.JNS081040
PMID:19408985
Abstract

OBJECT

Brain edema formation is a serious complication of ischemic stroke and can lead to mechanical compression of adjacent brain structures, cerebral herniation, and death. Furthermore, the space-occupying effect of edema impairs regional cerebral blood flow (rCBF), which is particularly important in the penumbra phase of stroke. In the present study, the authors evaluated the natural course of edema formation in the hyperacute phase of focal cerebral ischemia.

METHODS

Middle cerebral artery occlusion (MCAO) or a sham procedure was performed in rats within an MR imaging unit (in-bore occlusion). Both pre- and postischemic images could be compared on a pixel-by-pixel basis. The T2 relaxation time (T2RT), a marker for brain water content, was measured in regions of interest.

RESULTS

A significant increase in the T2RT was detectable as early as 20-45 minutes after MCAO. At this early time point the midline shift (MLS) amounted to 0.214 +/- 0.092 cm in the MCAO group and 0.061 +/- 0.063 cm in the sham group (p < 0.007). The T2RT and MLS increased linearly thereafter. Evans blue dye was intravenously injected in additional animals 20 and 155 minutes after MCAO. Extravasation of the dye was visible in all animals, indicating increased permeability of the blood-brain barrier.

CONCLUSIONS

Vasogenic brain edema occurs much earlier than expected following permanent MCAO and leads to MLS and mechanical compression of adjacent brain structures. Since compression effects can impair rCBF, early edema formation can significantly contribute to infarct formation and thus represents a promising target for neuroprotection.

摘要

目的

脑水肿形成是缺血性卒中的严重并发症,可导致邻近脑结构的机械性压迫、脑疝形成及死亡。此外,水肿的占位效应会损害局部脑血流量(rCBF),这在卒中的半暗带期尤为重要。在本研究中,作者评估了局灶性脑缺血超急性期脑水肿形成的自然病程。

方法

在大鼠的磁共振成像单元内(磁体腔内闭塞)进行大脑中动脉闭塞(MCAO)或假手术。缺血前后的图像可逐像素比较。在感兴趣区域测量作为脑含水量标志物的T2弛豫时间(T2RT)。

结果

早在MCAO后20 - 45分钟即可检测到T2RT显著增加。在此早期时间点,MCAO组的中线移位(MLS)为0.214±0.092 cm,假手术组为0.061±0.063 cm(p < 0.007)。此后T2RT和MLS呈线性增加。在MCAO后20分钟和155分钟对另外的动物静脉注射伊文思蓝染料。在所有动物中均可见染料外渗,表明血脑屏障通透性增加。

结论

永久性MCAO后血管源性脑水肿的发生比预期早得多,并导致MLS及对邻近脑结构的机械性压迫。由于压迫效应可损害rCBF,早期脑水肿形成可显著促进梗死灶形成,因此是神经保护的一个有前景的靶点。

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