Blood-brain barrier disruption, edema formation, and apoptotic neuronal death following cold injury.
The temporal pattern of brain edema and apoptosis following cold injury was investigated. Extravasation of Evans blue from the disrupted blood-brain barrier (BBB) maximized immediately after injury and returned to the control level at 24 h. However, water content increased up to 24 h and was maintained at a higher level than the control at 72 h. Apoptotic cells as detected by in situ end labeling were observed in the entire lesion at 24 h. At 72 h after injury, these apoptotic cells were observed in the margin of the lesion, but not in the core. These results suggest that apoptosis contributes to neuronal damage following cold injury and may result from the development of vasogenic edema.
Murakami
K
K
Department of Neurological Surgery, School of Medicine, University of California, San Francisco, USA.
Kondo
T
T
Chan
P H
PH
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001812:Blood-Brain Barrier / Q000502:physiology*; D001929:Brain Edema / Q000473:pathology / Q000503:physiopathology*; D003080:Cold Temperature; D005821:Genetic Techniques; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009474:Neurons / Q000473:pathology*