van den Bergh Walter M, Zuur J Karel, Kamerling Niels A, van Asseldonk Jan Thies H, Rinkel Gabriël J E, Tulleken Cornelis A F, Nicolay Klaas
Department of Neurosurgery, Experimental In Vivo Nuclear Magnetic Resonance and Neurology, University Medical Center Utrecht, The Netherlands.
J Neurosurg. 2002 Aug;97(2):416-22. doi: 10.3171/jns.2002.97.2.0416.
Ischemia-induced tissue depolarizations probably play an important role in the pathophysiology of cerebral ischemia caused by parent vessel occlusion. Their role in ischemia caused by subarachnoid hemorrhage (SAH) remains to be investigated. The authors determined whether ischemic depolarizations (IDs) or cortical spreading depressions (CSDs) occur after SAH, and how these relate to the extent of tissue injury measured on magnetic resonance (MR) images. In addition, they assessed whether administration of MgSO4 reduces depolarization time and lesion volume.
By means of the endovascular suture model, experimental SAH was induced in 52 rats, of which 37 were appropriate for analysis, including four animals that underwent sham operations. Before induction of SAH, serum Mg++ levels were measured and 90 mg/kg intravascular MgSO4 or saline was given. Extracellular direct current potentials were continuously recorded from six Ag/AgCl electrodes, before and up to 90 minutes following SAH, after which serum Mg++ levels were again measured. Next, animals were transferred to the MR imaging magnet for diffusion-weighted (DW) MR imaging. Depolarization times per electrode were averaged to determine a mean depolarization time per animal. No depolarizations occurred in sham-operated animals. Ischemic depolarizations occurred at all electrodes in all animals after SAH. Only two animals displayed a single spreading depression-like depolarization. The mean duration of the ID time was 41 +/- 25 minutes in the saline-treated controls and 31 +/- 30 minutes in the Mg++-treated animals (difference 10 minutes: p = 0.31). Apparent diffusion coefficient (ADC) maps of tissue H2O, obtained using DW images approximately 2.5 hours after SAH induction, demonstrated hypointensities in both hemispheres, but predominantly in the ipsilateral cortex. No ADC abnormalities were found in sham-operated animals. The mean lesion volume, as defined on the basis of a significant ADC reduction, was 0.32 +/- 0.42 ml in saline-treated controls and 0.11 +/- 0.06 ml in Mg++-treated animals (difference 0.21 ml; p = 0.045). Serum Mg++ levels were significantly elevated in the Mg++-treated group.
On the basis of their data, the authors suggest that CSDs play a minor role, if any, in the acute pathophysiology of SAH. Administration of Mg++ reduces the cerebral lesion volume that is present during the acute period after SAH. The neuroprotective value of Mg++ after SAH may, in part, be explained by a reduction in the duration of the ID of brain cells.
缺血诱导的组织去极化可能在大脑主要血管闭塞所致脑缺血的病理生理过程中发挥重要作用。其在蛛网膜下腔出血（SAH）所致缺血中的作用仍有待研究。作者确定SAH后是否会发生缺血性去极化（ID）或皮质扩散性抑制（CSD），以及这些与磁共振（MR）图像上测量的组织损伤程度有何关系。此外，他们评估了硫酸镁给药是否能缩短去极化时间并减小病变体积。
通过血管内缝合模型，在52只大鼠中诱导实验性SAH，其中37只适合分析，包括4只接受假手术的动物。在诱导SAH前，测量血清镁离子水平，并给予90mg/kg血管内硫酸镁或生理盐水。在SAH前及SAH后长达90分钟，用六个银/氯化银电极连续记录细胞外直流电位，之后再次测量血清镁离子水平。接下来，将动物转移至MR成像磁体进行扩散加权（DW）MR成像。计算每个电极的去极化时间平均值，以确定每只动物的平均去极化时间。假手术动物未发生去极化。SAH后所有动物的所有电极均出现缺血性去极化。仅两只动物出现单次类似扩散性抑制的去极化。生理盐水处理的对照组ID时间平均持续41±25分钟，镁离子处理的动物为31±30分钟（差异10分钟；p = 0.31）。在SAH诱导后约2.5小时使用DW图像获得的组织水分子表观扩散系数（ADC）图显示，双侧半球均有低信号，但主要在同侧皮质。假手术动物未发现ADC异常。根据显著的ADC降低定义的平均病变体积，生理盐水处理的对照组为0.32±0.42ml，镁离子处理的动物为0.11±0.06ml（差异0.21ml；p = 0.045）。镁离子处理组的血清镁离子水平显著升高。
基于他们的数据，作者认为CSD在SAH的急性病理生理过程中即使有作用也很小。镁离子给药可减小SAH急性期出现的脑病变体积。SAH后镁离子发挥神经保护作用的部分原因可能是脑细胞ID持续时间缩短。
