Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats
- PDF / 1,210,700 Bytes
- 9 Pages / 595.276 x 790.866 pts Page_size
- 67 Downloads / 235 Views
ORIGINAL ARTICLE
Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats Jinbing Zhao & Zhi Chen & Guohua Xi & Richard F. Keep & Ya Hua
Received: 29 April 2014 / Revised: 5 June 2014 / Accepted: 5 June 2014 # Springer Science+Business Media New York 2014
Abstract 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 T2weighted 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±3.0 vs. 9.9±0.2 mm3 in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7±3.4 vs. 9.0±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. Keywords Deferoxamine . Hydrocephalus . Lateral fluid percussion . Traumatic brain injury
Introduction Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in children and adolescents [1]. Each year in the J. Zhao : Z. Chen : G. Xi : R. F. Keep : Y. Hua (*) Department of Neurosurgery, University of Michigan, R5018 Biomedical Science Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA e-mail: [email protected]
United States, approximately 1.7 million people suffer a TBI [2]. Ventricular dilation is a frequent phenomenon in TBI patients and may present in follow up exam and turn into post-traumatic hydrocephalus (PTH). Marmarou and colleagues [3] reported that 44 % of severe head injury survivors develop post-traumatic ventriculomegaly, among which about half of the survivors were classified as PTH. The incidence of PTH varies between studies from 0.7 % to as high as 29 % [4, 5]. PTH has been recognized as an indicator of worse outcome after TBI [6]. However, the mechanisms of early and late ventricular dilation are still not well understood. Intracranial bleeding is a common and serious consequence of TBI [7]. Magnetic resonance imaging (MRI) has shown a preponderance of hemorrhagic lesions compared to ischemic lesions during the acute phase after TBI. Thus, a study found that 56 % of TBI patients had at least one intracranial bleed [8] and another showed that patients with greater initial total hemorrhagic contusion volume had more severe chronic brain atrophy [9]. Our previous studies in intrac
Data Loading...
