자발성 고혈압 쥐에서 만성 뇌 혈류 저하가 중대뇌동맥 폐색에 의한 세포 손상에 미치는 영향

Abstract

Background: 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±349.93) when com-pared with those in the sham operation group (1132.08±1363.64) (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.