The Role of Intracranial Pressure and Subarachnoid Blood Clots in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats
The Role of Intracranial Pressure and Subarachnoid Blood Clots in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats
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DOI：
10.1016/j.wneu.2019.05.009
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发表时间：
2019-09-01
影响因子：
2
通讯作者：
Ohkuma, Hiroki
中科院分区：
文献类型：
--
作者：
Naraoka, Masato;Fumoto, Toshio;Ohkuma, Hiroki
目的：蛛网膜下腔出血（SAH）后早期脑损伤被认为是导致预后不良的主要因素，据信是由颅内压（ICP）升高和/或蛛网膜下腔血块（SBC）本身的存在引起的。本研究的目的是探讨在细胞凋亡或水肿存在的情况下ICP或SBC是否对神经功能缺损更重要。方法：将50只大鼠分为3组：血管内穿孔SAH模型（SAH组）、小脑延髓池盐水注射模型（盐水注射组）和小脑延髓池假注射模型（假注射组）。对ICP、血块体积分级、神经元凋亡、脑含水量（脑水肿）和神经功能缺损之间的相关性进行统计分析。结果：在SAH组中，ICP和血块体积的增加均与神经元凋亡和脑水肿相关。在盐水注射组中，ICP增加与细胞凋亡相关，但与脑水肿无关。 SAH组神经元凋亡（r = 0.75；P < 0.01）和脑水肿（r = 0.89；P < 0.01）与神经功能缺损独立相关。 结论：本研究提示神经元凋亡主要是由ICP升高引起的，而脑水肿是由SBC引起的，并且在SBC存在的情况下ICP升高会加重脑水肿。脑水肿可能影响神经功能缺损，但单独的细胞凋亡影响可能较小。不仅ICP，SBC似乎对SAH急性期的脑损伤也很重要。
OBJECTIVE: Early brain injury after subarachnoid hemorrhage (SAH), which is considered a main factor leading to poor outcome, is believed to be caused by the increase of intracranial pressure (ICP) and/or the presence of subarachnoid blood clots (SBC) itself. The purpose of this study was to examine whether ICP or SBC is more important to neurologic deficit in the presence of apoptosis or edema.METHODS: A total of 50 rats were allocated to 3 groups: an endovascular perforation SAH model (the SAH group), a cisterna magna saline injection model (the saline injection group), and a cisterna magna sham injection model (the sham injection group). Statistical analysis of correlations among the ICP, the grade of clot volume, neuronal apoptosis, brain water content (brain edema), and neurologic deficit was performed.RESULTS: In the SAH group, each of increased ICP and clot volume was correlated with neuronal apoptosis and brain edema. In the saline injection group, increased ICP was associated with apoptosis, but it did not correlate with brain edema. Neuronal apoptosis (r = 0.75; P < 0.01) and brain edema (r = 0.89; P < 0.01) correlated independently with neurologic deficit in the SAH group.CONCLUSIONS: The present study suggests that neuronal apoptosis is caused mainly by increased ICP, whereas brain edema is induced by SBC, and increased ICP could aggravate it in the presence of SBC. Brain edema could affect neurologic deficit, but apoptosis alone may be less influential. Not only ICP but also SBC seem important for brain damage in the acute stage of SAH.