Thal Serge C, Sporer Sonja, Klopotowski Mariusz, Thal Simone E, Woitzik Johannes, Schmid-Elsaesser Robert, Plesnila Nikolaus, Zausinger Stefan
Institute for Surgical Research, University of Munich Medical Center-Grosshadern, Munich, Germany.
J Neurosurg. 2009 Nov;111(5):988-94. doi: 10.3171/2009.3.JNS08412.
Global cerebral edema is an independent risk factor for early death and poor outcome after subarachnoid hemorrhage (SAH). In the present study, the time course of brain edema formation, neurological deficits, and neuronal cell loss were investigated in the rat filament SAH model.
Brain water content and neurological deficits were determined in rats randomized to sham (1-, 24-, or 48-hour survival), SAH by endovascular perforation (1-, 24-, or 48-hour survival), or no surgery (control). The neuronal cell count (CA1-3) was quantified in a separate set of SAH (6-, 24-, 48-, or 72-hour survival) and shamoperated animals.
Brain water content increased significantly 24 (80.2 +/- 0.4% [SAH] vs 79.2 +/- 0.1% [sham]) and 48 hours (79.8 +/- 0.2% [SAH] vs 79.3 +/- 0.1% [sham]) after SAH. The neuroscore was significantly worse after SAH (33 +/- 15 [24 hours after SAH] vs 0 +/- 0 points [sham]) and correlated with the extent of brain edema formation (r = 0.96, p < 0.001). No hippocampal damage was present up to 72 hours after SAH.
Brain water content and neurological dysfunction reached a maximum at 24 hours after SAH. This time point, therefore, seems to be optimal to test the effects of therapeutic interventions on brain edema formation. Neuronal cell loss was not present in CA1-3 up to 72 hours of SAH. Therefore, morphological damage needs to be evaluated at later time points.
全脑水肿是蛛网膜下腔出血（SAH）后早期死亡和不良预后的独立危险因素。在本研究中，我们在大鼠丝线SAH模型中研究了脑水肿形成、神经功能缺损和神经元细胞丢失的时间进程。
将大鼠随机分为假手术组（存活1、24或48小时）、血管内穿刺SAH组（存活1、24或48小时）或未手术组（对照组），测定脑含水量和神经功能缺损情况。在另一组SAH（存活6、24、48或72小时）和假手术动物中对神经元细胞计数（CA1-3）进行定量分析。
SAH后24小时（SAH组为80.2±0.4%，假手术组为79.2±0.1%）和48小时（SAH组为79.8±0.2%，假手术组为79.3±0.1%）脑含水量显著增加。SAH后神经评分显著更差（SAH后24小时为33±15分，假手术组为0±0分），且与脑水肿形成程度相关（r = 0.96，p < 0.001）。SAH后72小时内未出现海马损伤。
SAH后24小时脑含水量和神经功能障碍达到峰值。因此，这个时间点似乎是测试治疗干预对脑水肿形成影响的最佳时机。SAH后72小时内CA1-3区未出现神经元细胞丢失。因此，需要在更晚的时间点评估形态学损伤。
