Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats

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• 作者：Jinbing Zhao (1)
  Zhi Chen (1)
  Guohua Xi (1)
  Richard F. Keep (1)
  Ya Hua (1)
  
• 关键词：Deferoxamine ; Hydrocephalus ; Lateral fluid percussion ; Traumatic brain injury
• 刊名：Translational Stroke Research
• 出版年：2014
• 出版时间：October 2014
• 年：2014
• 卷：5
• 期：5
• 页码：586-594
• 全文大小：1,165 KB
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• 作者单位：Jinbing Zhao (1)
  Zhi Chen (1)
  Guohua Xi (1)
  Richard F. Keep (1)
  Ya Hua (1)
  
  1. Department of Neurosurgery, University of Michigan, R5018 Biomedical Science Research Building, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA
  
• ISSN：1868-601X

文摘

Acute post-traumatic ventricular dilation and hydrocephalus are relatively frequent consequences of traumatic brain injury (TBI). Several recent studies have indicated that high iron levels in brain may relate to hydrocephalus development after intracranial hemorrhage. However, the role of iron in the development of post-traumatic hydrocephalus is still unclear. This study was to determine whether or not iron has a role in hydrocephalus development after TBI. TBI was induced by lateral fluid-percussion in male Sprague–Dawley rats. Some rats had intraventricular injection of iron. Acute hydrocephalus was measured by magnetic resonance T2-weighted imaging and brain hemorrhage was determined by T2* gradient–echo sequence imaging and brain hemoglobin levels. The effect of deferoxamine on TBI-induced hydrocephalus was examined. TBI resulted in acute hydrocephalus at 24?h (lateral ventricle volume: 24.1?±-.0 vs. 9.9?±-.2?mm3 in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7?±-.4 vs. 9.0?±-.6?mm3 in saline group). Deferoxamine treatment attenuated TBI-induced hydrocephalus and heme oxygenase-1 upregulation. In conclusion, iron may contribute to acute hydrocephalus after TBI.