Abstract
The morphological changes after cardiac arrest in the hippocampus region were evaluated by light and electron microscopy using a mouse cardiac-arrest model, in which the major cardiac vessels are compressed for 5 min followed by recirculation. Degenerating cells first appeared in the hippocampal CA1 and dentate gyrus on day 1, and then increased in number with time on days 2 days, 4 and 7 after recirculation. The in situ nick-end labeling (TUNEL) technique identified apoptotic pyramidal cells and granule cells on day 1 which then increased with time. At the ultrastructural level, cell shrinkage and nuclear condensation of the pyramidal cells and granule cells were observed in the CA l and dentate gyrus. The ischemia-reperfusion activated the proliferation of microglial cells in the hippocampal region. The microglial cells were often seen to adhere to degenerating neurons in the CA l region and dentate gyrus suggesting that they may phagocytose the degenerating neurons. The present study clearly shows the regional differences in neuronal vulnerability in mice brain following ischemia injury induced with the cardiac arrest model., Further study of the mechanisms of selective delayed neuronal cell death in the hippocampus is warranted.
