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Submitted on November 6, 2004
From the Center for Human Growth and Development (J.S., B.F.) and the Department of Neurosurgery (G.X., Y.H., T.S.), University of Michigan, Ann Arbor; Department of Pediatric Health Care, Children’s Hospital, Zhejiang University School of Medicine, China (J.S.); and Department of Psychology (T.S.), University of Texas, Austin. * To whom correspondence should be addressed. E-mail: truefelt{at}umich.edu.
Background and Purpose--Iron contributes to brain injury after intracerebral hemorrhage (ICH). Because ICH may occur in the context of iron deficiency anemia (IDA), a common nutritional disorder, the purpose of this study was to determine whether IDA in rats affects brain edema, functional behavior, and changes in brain iron-handling proteins after ICH. Methods--Six-week-old male rats (n=75) were randomized to non-IDA or IDA groups and provided iron-sufficient or -deficient diets, respectively. After 1 month, 100 µL autologous blood was infused into the right basal ganglia (BG). Brains removed at days 1, 3, 7, and 28 after ICH were assessed for regional brain water content and BG transferrin and transferrin receptor concentrations (Western blotting). Sensorimotor measures of functional recovery were assessed. Results--Brain water content was increased for IDA versus non-IDA in injured cortex and BG at day 3 (P<0.05). IDA rats had impaired left forepaw placing and more asymmetric forelimb use versus non-IDA after ICH (P<0.05). Transferrin and transferrin receptor concentrations in the BG were increased for IDA versus non-IDA within the first week (P<0.05). Conclusions--Rats with IDA have greater brain edema, poorer sensorimotor outcome, and a greater expression of iron regulatory proteins than non-IDA rats after ICH, suggesting brain iron status is a determinant of injury severity and recovery.
Accepted on December 7, 2004
Intracerebral Hemorrhage in the Iron-Deficient Rat
Jie Shao MD;
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