Michenfelder J D, Milde J H
Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905.
J Cereb Blood Flow Metab. 1990 Jan;10(1):71-6. doi: 10.1038/jcbfm.1990.9.
Following a period of complete global cerebral ischemia and reperfusion there ensues a low flow state referred to as the delayed postischemic hypoperfusion state. It is unknown whether this low flow state contributes to neuronal injury or whether the magnitude of hypoperfusion correlates with the duration of ischemia. The latter question was addressed in 20 dogs in which complete global ischemia was induced by cerebrospinal fluid (CSF) compression for periods of 3, 9, 12, or 18 min. Following reperfusion, CBF (by sagittal sinus outflow) and CMRO2 were determined for 90 min, and results were correlated with the duration of ischemia. At 90 min postischemia the magnitude of decrease in CBF correlated crudely with the duration of ischemia (r = -0.67, p less than 0.01). For CMRO2 correlation of the magnitude of decrease with the duration of ischemia was more evident (r = -0.74, p less than 0.001). Furthermore, the postischemic ratio of CBF to CMRO2 was virtually identical for all dog groups regardless of the ischemic time. The adequacy of the ratio of CBF to CMRO2 was reflected by adequate oxygen levels in the sagittal sinus blood of all dogs. The authors conclude that the delayed postischemic hypoperfusion state is probably not an important determinant of neuronal injury since its magnitude appears to be primarily determined by the metabolic needs of the brain.
在经历一段完全性全脑缺血和再灌注后，会出现一种低流量状态，称为缺血后延迟性低灌注状态。尚不清楚这种低流量状态是否会导致神经元损伤，也不清楚低灌注的程度是否与缺血持续时间相关。后一个问题在20只狗身上进行了研究，通过脑脊液（CSF）压迫诱导全脑完全缺血3、9、12或18分钟。再灌注后，测定90分钟的脑血流量（通过矢状窦流出）和脑氧代谢率（CMRO2），并将结果与缺血持续时间相关联。在缺血后90分钟，脑血流量降低的幅度与缺血持续时间大致相关（r = -0.67，p < 0.01）。对于脑氧代谢率，降低幅度与缺血持续时间的相关性更为明显（r = -0.74，p < 0.001）。此外，无论缺血时间如何，所有狗组缺血后脑血流量与脑氧代谢率的比值实际上是相同的。所有狗矢状窦血中充足的氧水平反映了脑血流量与脑氧代谢率比值的充足性。作者得出结论，缺血后延迟性低灌注状态可能不是神经元损伤的重要决定因素，因为其程度似乎主要由大脑的代谢需求决定。
