Abstract
Cerebral ischemia was produced in anesthetized cats using a neck tourniquet, which diminished cortical blood flow to less than 2 ml/100 g/min and depleted levels of ATP throughout the brain. Following a 30-min insult, cortical flow measured with H2 electrodes returned nearly to control, but subsequently decreased to 14-47% of control values. Despite this secondary hypoperfusion, ATP levels adjacent to the H2 electrode were restored to 75% of normal during the 2-h recirculation period. Therefore, this degree of hypoperfusion did not cause a secondary failure of energy metabolism. Following a 60-min insult, impaired reperfusion prevented the regeneration of brain ATP. However, preischemic bilateral craniectomies significantly improved recovery of blood flow and ATP levels following 60 min of ischemia. Therefore, in the present model, insufficient reflow is a primary factor limiting recovery of energy metabolism. Further, surgical decompression prevented the occurrence of "no reflow" caused by 60 min of ischemia.
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