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Bockhorst, K.H.* ; Narayana, P.A.* ; Dulin, J.* ; Liu, R.* ; Rea, H.C.* ; Hahn, K.R. ; Wosik, J.* ; Perez-Polo, J.R.*

Normobaric hyperoximia increases hypoxia-induced cerebral injury: DTI study in rats.

J. Neurosci. Res. 88, 1146-1156 (2010)
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Perinatal hypoxia affects normal neurological development and can lead to motor, behavioral and cognitive deficits. A common acute treatment for perinatal hypoxia is oxygen resuscitation (hyperoximia), a controversial treatment. Magnetic resonance imaging (MRI), including diffusion tensor imaging (DTI), was performed in a P7 rat model of perinatal hypoxia to determine the effect of hyperoximia. These studies were performed on two groups of animals: 1) animals which were subjected to ischemia followed by hypoxia (HI), and 2) HI followed by hyperoximic treatment (HHI). Lesion volumes on high resolution MRI and DTI derived measures, fractional anisotropy (FA), mean diffusivity (MD), and axial and radial diffusivities (lambda(l) and lambda(t), respectively) were measured in vivo one day, one week, and three weeks after injury. Most significant differences in the MRI and DTI measures were found at three weeks after injury. Specifically, three weeks after HHI injury resulted in significantly larger hyperintense lesion volumes (95.26 +/- 50.42 mm(3)) compared to HI (22.25 +/- 17.62 mm(3)). The radial diffusivity lambda(t) of the genu of corpus callosum was significantly larger in HHI (681 +/- 330 x 10(-6) mm(2)/sec) than in HI (486 +/- 96 x 10(-6) mm(2)/sec). Over all, most significant differences in all the DTI metrics (FA, MD, lambda(t), lambda(l)) at all time points were found in the corpus callosum. Our results suggest that treatment of perinatal hypoxia with normobaric oxygen does not ameliorate, but exacerbates damage.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter hyperoxia; ischemia; rodents; diffusivity; MRI
ISSN (print) / ISBN 0360-4012
e-ISSN 1097-4547
Quellenangaben Band: 88, Heft: 5, Seiten: 1146-1156 Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Wilmington, DE
Begutachtungsstatus Peer reviewed