Postischemic canine cerebral blood flow is coupled to cerebral metabolic rate

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO₂ was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion. Following reperfusion and onset of the low-flow state, which stabilized at 45 min postischemia, control normothermic (37°C) measurements of CBF and CMRO₂ were determined. Thereafter, femoral arterial blood was circulated through a heat exchanger (42.5°C), and brain temperature was increased to 40°C and measurements were repeated. The brain was then cooled back to 37°C for a final set of normothermic measurements. Thereafter, brain biopsies were taken to determine the energy state of the brain. CMRO₂ changed ∼6%/°C. CBF paralleled the change in CMRO₂. Accordingly, the ratio of CBF to CMRO₂ remained constant throughout at a value of 8 to 9, demonstrating maintained coupling. The brain energy state was normal at the end of the study. The authors conclude that postischemic CBF is modulated by the brain's metabolic needs.