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Neuropathological Findings of Neonatal Mice Following Hypoxic Encephalopathy
Author(s) -
Yoshioka Hiroshi,
Sato Noriko,
Okano Sozo,
Yamazoe Ichiro,
Nishiki Tetsuo,
Kotani Hiromi,
Sawada Tadashi
Publication year - 1993
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.1993.tb00210.x
Subject(s) - periventricular leukomalacia , subependymal zone , medicine , encephalomalacia , hypoxic ischemic encephalopathy , pathology , hypoxia (environmental) , pathogenesis , encephalopathy , lesion , ischemia , neuropathology , brain damage , cardiology , biology , oxygen , disease , chemistry , pregnancy , genetics , organic chemistry , gestational age
One‐day‐old mice were subjected to hypoxia by 8‐hour exposure to a 5% oxygen, 95% nitrogen mixture. The brains from ten surviving mice with moderate brain hemorrhage were microscopically examined at 36 and 60 hours after the hypoxic event. These brains showed the coexistence of parasagittal cerebral injury, periventricular leukomalacia, multicystic encephalomalacia and subependymal germinolysis. Parasagittal cerebral injury is regarded as the principal ischemic lesion of the full‐term human infant, and periventricular leukomalacia as that of the premature infant. These results suggest the important role of hypoxia/ischemia in the pathogenesis of subependymal germinolysis and regional differences in maturation between mouse and human brain.