Chronic cerebral hypoperfusion and reperfusion injury of restoration of normal perfusion pressure contributes to the neuropathological changes in rat brain

Jian Hai, Qi Lin, Shi-Ting Li, Qing-Gang Pan
Brain Research. Molecular Brain Research 2004 July 26, 126 (2): 137-45
Restoration of normal perfusion pressure after resection of cerebral arteriovenous malformations (AVMs) is sometimes complicated by unexplained postoperative brain swelling and/or intracranial hemorrhage, which has been termed normal perfusion pressure breakthrough (NPPB). The precise mechanism of NPPB is still unclear. In this study, we investigated the time courses of blood-brain barrier (BBB) disruption, water content, neuronal apoptosis, myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in the brain during restoration of normal perfusion pressure in a new rat model of chronic cerebral hypoperfusion associated with AVMs. Male Sprague-Dawley rats were randomly divided into either a sham-operated group, a control group, or a model group with reperfusion assessed at 1, 12, 24 and 72 h after restoration of normal perfusion pressure. BBB disruption was judged by extravasation of Evans blue (EB) dye. We observed that EB and water content in rat brains of the model group with reperfusion were significantly increased compared with the other groups. The most predominant increase occurred at 1 h after reperfusion, and the next at 24 h after reperfusion, representing biphasic changes which are similar to the pathological processes of acute cerebral ischemia/reperfusion injury. There was no difference of the percentage of apoptotic cells in rat brains between the sham-operated group and the control group using flow cytometry. No prominent apoptotic cells were found in the model group with reperfusion at 1 h. However, the percentage of apoptotic cells increased significantly in rat brains of the model group with reperfusion at 12 h, peaked at 24 h, and decreased at 72 h after reperfusion. Apoptotic cells were confirmed with electron microscopy and terminal deoxynuleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). A significant enhancement of MPO activity in combination with reduction of SOD activity was seen at 12, 24 and 72 h in rat brains of the model group with reperfusion. Our data indicates that reperfusion after restoration of normal perfusion pressure with chronic cerebral hypoperfusion lead to secondary neuronal damage which may associate with cerebral ischemia/reperfusion injury.


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