Early cellular events in the penumbra of human spontaneous intracerebral hemorrhage.
Early cellular events in the penumbra of human spontaneous intracerebral hemorrhage.
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DOI：
10.1016/s1052-3057(99)80032-9
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发表时间：
1999-01-01
期刊：
影响因子：
--
通讯作者：
Clayton, J A
中科院分区：
文献类型：
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作者：
Mackenzie, J M;Clayton, J A
自发性脑出血具有很高的发病率和死亡率，但其治疗仍然存在争议，部分原因是对周围脑损伤的发病机制和时间尺度缺乏了解。本研究旨在阐明自发性脑内血肿周围的细胞反应及其与血肿持续时间和血肿体积的关系，从而为制定治疗策略提供进一步的数据。用免疫组织化学方法对33例自发性脑出血死亡患者血肿边缘脑组织和13例正常对照脑组织进行了热休克蛋白、金属硫蛋白和各种神经元、神经胶质细胞、巨噬细胞和内皮细胞标志物的免疫组织化学研究。血肿体积通过计算机断层扫描(CT)和尸检测量计算，而血肿年龄则根据临床记录估计。结果表明，细胞事件是时间依赖的，但与血肿量无关，早在出血后5小时就可在神经元、神经胶质细胞和内皮细胞中发现。外周巨噬细胞在第5天开始浸润。结果表明，血肿缺血半暗带再通的治疗窗口不到5小时，尽管梗塞核心在1-3天内进展到半暗带周围表明有更宽的细胞保护窗口。血脑屏障破裂引起的水肿也在5小时内被发现，及时治疗可以减少血肿的占位效应，并可能减少发病率和死亡率。
Spontaneous intracerebral hemorrhage causes high morbidity and mortality rates, and yet its treatment remains controversial, partly because of a poor understanding of the pathogenesis and timescale of injury in the surrounding brain. This study was undertaken to clarify the cellular reactions around human spontaneous intracerebral hematomas and relate these to hematoma duration and volume, in order to provide further data that might aid the development of therapeutic strategies. Brain tissue from the margin of the hematoma in 33 fatal cases of spontaneous intracerebral hemorrhage and corresponding tissue from 13 normal controls was studied using immunohistochemistry for heat-shock proteins, metallothionein, and various neuronal, glial, macrophage, and endothelial markers. Hematoma volumes were calculated from computed tomographic (CT) scans and autopsy measurements, whereas hematoma age was estimated from clinical records. The results showed that cellular events are time dependent, but not related to hematoma volume, and are identifiable in neurons, glia, and endothelium as early as 5 hours after hemorrhage. Peripheral macrophage infiltration begins at 5 days. The results suggest that the therapeutic window in humans for reperfusion of the ischemic penumbra of a hematoma is less than 5 hours, although progression of the infarcted core to the penumbral periphery within 1 to 3 days suggests a wider cytoprotective window. Edema, caused by blood-brain barrier breakdown, was also identified at 5 hours, and prompt treatment of this may reduce the space-occupying effects of the hematoma and, possibly, the morbidity and mortality.