correlation between cerebrospinal fluid iron levels and cerebral tissue damage following experimental head injury in rats

نویسندگان

فرزاد سعدلو پاریزی

f saadlou . [email protected] محمد علی خلیلی

ma khalili علی حاذقی

a hazeghi

چکیده

introduction: in iran, thousands of young individuals become victims of head injury annually. head injury can damage neuronal cells which may in turn complicate the recovery of the patients. also, the increase of iron in cerebrospinal fluid (csf) following head injury may contribute to the hypoxic-ischemia brain damage by catalyzing the formation of free radicals (harber-weiss rection). the object was to study the correlation between the level of iron in csf with cerebral tissue damage after experimental head injury in adult male rats. methods: a total of 27 wistar rats were randomly divided into 3 groups of control (n=7), experimental i (n=9), and experimental ii (n=11). head injury was induced with a 300g weight dropped on the skull from a distance of 1 meter. csf samples were withdrawn from controls with insertion of a hamilton needle throught atlanto-ocipital (oa) membrane. also, csfs were collected from experimental animals i and ii at 30 min and 60 min after induction of head injury, respectively. all csf samples were measured with atomic absorption spectrometry. also, biopsy samples from parietal lobe of brain were fixed in 10% formalin and stained with hemotoxylin-eosin for morphological evaluation. results: the level of iron in csf of control group was 2.95±31ppm. the level of iron in experimetanl groups of i and ii increased to 6.14±1.01 (p>0.05) and 14.72±2.94 (p<0.001), respectively. the cerebral tissue of group i consisted of abnormal dark neurons which were scattered among normal neurons. however, the majority of neuronal cells were damaged in experimental group ii. conclusion: the results showed that the level of iron in csf as well as neuronal cell architecture was time-dependent after experimental head injury. this may cause a non-reversible brain injury with release of free radicals in csf following head injury.

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