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自发性高血压大鼠脑出血后的脑损伤。

Brain injury after intracerebral hemorrhage in spontaneously hypertensive rats.

机构信息

Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan 48109-2200, USA.

出版信息

J Neurosurg. 2011 Jun;114(6):1805-11. doi: 10.3171/2011.1.JNS101530. Epub 2011 Feb 4.

Abstract

OBJECT

Hypertension is the main cause of spontaneous intracerebral hemorrhages (ICHs), but the effects of hypertension on ICH-induced brain injury have not been well studied. In this study, the authors examined ICH-induced brain injury in spontaneously hypertensive rats (SHRs).

METHODS

This 2-part study was performed in 12-week-old male SHRs and Wistar Kyoto (WKY) rats. First, the rats received an intracaudate injection of 0.3 U collagenase, and hematoma sizes were determined at 24 hours. Second, rats were injected with 100 μl autologous whole blood into the right basal ganglia. Brain edema, neuronal death, ferritin expression, microglia activation, and neurological deficits were examined.

RESULTS

Hematoma sizes were the same in SHR and WKY rats 24 hours after collagenase injection. The SHRs had greater neuronal death and neurological deficits after blood injection. Intracerebral hemorrhage also resulted in higher brain ferritin levels and stronger activation of microglia in SHRs. However, perihematomal brain edema was the same in the SHRs and WKY rats.

CONCLUSIONS

Moderate chronic hypertension resulted in more severe ICH-induced neuronal death and neurological deficits, but did not exaggerate hematoma enlargement and perihematomal brain edema in the rat ICH models.

摘要

目的

高血压是自发性脑出血(ICH)的主要原因,但高血压对ICH 引起的脑损伤的影响尚未得到很好的研究。在这项研究中,作者研究了自发性高血压大鼠(SHR)的 ICH 引起的脑损伤。

方法

这项由两部分组成的研究在 12 周龄雄性 SHR 和 Wistar Kyoto(WKY)大鼠中进行。首先,大鼠接受尾状核内 0.3U 胶原酶注射,24 小时后测定血肿大小。其次,大鼠将 100μl 自体全血注入右侧基底节。检查脑水肿、神经元死亡、铁蛋白表达、小胶质细胞激活和神经功能缺损。

结果

胶原酶注射后 24 小时,SHR 和 WKY 大鼠的血肿大小相同。脑出血后,SHR 的神经元死亡和神经功能缺损更大。脑出血还导致 SHR 脑内铁蛋白水平升高和小胶质细胞激活增强。然而,SHR 和 WKY 大鼠的血肿周围脑水肿相同。

结论

中度慢性高血压导致更严重的 ICH 引起的神经元死亡和神经功能缺损,但在大鼠 ICH 模型中并未夸大血肿扩大和血肿周围脑水肿。

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