Apoptosis has been known to contribute to neuronal death following a variety of brain insults. However, the role of vasogenic brain edema in neuronal apoptosis is unknown. We studied the temporal pattern of brain edema and neuronal apoptosis following cold injury. Cold injury-induced brain edema, which was detected by the increased water content in the injured hemisphere, reached its maximum level at 24 h and remained there at 72 h, whereas the blood brain barrier breakdown detected by Evans Blue extravasation returned to the control value by 24 h after injury. Terminal deoxynucleotidyl transferasemediated uridine-5'-triphosphate-biotin nick end labeling (TUNEL)-positive apoptotic cells were scattered in the center of the lesion at 1 h and were dispersed over the cold lesion at 24 h. The number of these TUNEL-positive cells was maximized in the periphery but decreased in the center at 72 h after cold injury. We postulate that secondary neuronal damage occurred not only through necrotic, but also apoptotic pathways, and that apoptotic neuronal death may result from vasogenic edema development and may contribute to the expansion of the lesion in both the acute and delayed phases after cold injury.
- Blood-brain barrier breakdown
- Cold injury
- Neuronal apoptosis
- Vasogenic edema
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