자발성고혈압쥐에서만성뇌혈류저하가중대뇌동맥폐색에의한세포손상에미치는영향

Abstract

Department of Neurology, National Health Insurance Corporation Ilsan Hospital Department of Neurology, Yonsei University College of Medicine* B a c k g ro u n d: An ischemic stroke can result from various mechanisms such as atherothrombosis, cardioem-bolism or hemodynamic compromise. It has been reported that patients with atherothrombotic stroke have lesssevere neurological deficits and smaller cerebral infarctions than those with cardioembolic strokes. When exposedto a sufficient but sublethal alteration of their environment, most living organisms acquire transient tolerance tosubsequent and other lethal environmental changes. Methods: We examined the effect of chronic cerebral hypop-erfusion on middel cerebral artery occlusion/reperfusion (MCAO/R)-induced cellular damage. Spontaneoushypertensive rats (SHR) that were bred for 4 weeks after bilateral common carotid artery ligation (BCAL) or shamoperation were subjected to MCAO/R using a nylon suture model. In paraffin sections obtained from aubjects ineach group, in situnick translation study were performed and number of dUTP incorporated cells were counted.Results: The number of positive cells in the in situnick translation study, which was taken as an indication of cel-lular injury, was significantly reduced in the chronic cerebral hypoperfusion group (166.33¡¾349.93) when com-pared with those in the sham operation group (1132.08¡¾1363.64) (p<0.05). Conclusions: The findings of thisstudy provide experimental evidence for the hypothesis that chronic sublethal cerebral hypoperfusion is protectivefor subsequent severe ischemic insults.