| ironjustice@aol.com 2006-03-03, 10:58 am |
| Long-term effects of experimental intracerebral hemorrhage: the role of
iron.
Hua Y, Nakamura T, Keep RF, Wu J, Schallert T, Hoff JT, Xi G
J Neurosurg. 2006 Feb ; 104(2): 305-12
OBJECT: Intracerebral hemorrhage (ICH) causes brain atrophy and
neurological deficits. The mechanisms of brain atrophy after ICH are
poorly understood, although recent evidence suggests that some
ICH-induced brain injury results from the products of hemoglobin
degradation, including iron. In this study the authors examine the role
of iron in brain atrophy and neurological deficits following ICH.
METHODS: Male Sprague-Dawley rats received an infusion of either 100
microl autologous whole blood or saline into the right caudate.
Hematoxylin and eosin staining was used for histological examination,
and iron levels and ferritin immunoreactivities were also examined.
Deferoxamine was used as an iron chelator. Over the duration of the
experiment, the rats underwent behavioral testing (forelimb placing,
forelimb use asymmetry, and corner turn tests). Brain atrophy in the
caudate with prolonged neurological deficits occurred after ICH.
Although partial functional recovery occurred with time, residual
neurological deficits were still detectable at 3 months postprocedure.
Iron accumulation and ferritin upregulation were present in the
ipsilateral caudate. Deferoxamine reduced brain atrophy and improved
behavioral outcomes, and it also reduced brain ferritin
immunoreactivity. CONCLUSIONS: An ICH results in an accumulation of
iron in the brain that is not cleared within 3 months and that
contributes to brain tissue loss and neurological deficits
posthemorrhage. Iron chelation may be a useful therapy for patients
with ICH.
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