Koch K A, Jackson D L, Schmiedl M, Rosenblatt J I
J Cereb Blood Flow Metab. 1984 Sep;4(3):343-9. doi: 10.1038/jcbfm.1984.51.
Radiolabeled 15-microns microspheres were used to examine alterations in regional CBF and cerebrovascular resistance in response to changes in arterial PCO2. Flow measurements were obtained before and 1-3 and 24 h after 12 min of total cerebral ischemia. Striking sensitivity of blood flow in all areas of the central nervous system was shown to changes in arterial PCO2 between 24 and 50 mm Hg during the control nonischemic period. Following 12 min of total cerebral ischemia, cerebrovascular resistance increased, producing a decrease in regional blood flow when the important controlling variables for CBF were held constant. One to 3 h after total cerebral ischemia, the effect of variations in arterial PCO2 on cerebral blood flow was almost completely abolished. Within 24 h after total cerebral ischemia, the sensitivity of CBF to changes in PCO2 was almost completely restored, whereas the secondary severe neurologic deficit remained. Therapeutic interventions following global cerebral ischemia, designed to ameliorate the "no-reflow" phenomenon and minimize residual ischemic neurologic damage, must take into account this marked early post-ischemic reduction in sensitivity to normally potent cerebrovasodilatory influences.
放射性标记的15微米微球被用于检测动脉血二氧化碳分压（PCO2）变化时局部脑血流量（CBF）和脑血管阻力的改变。在全脑缺血12分钟之前、之后1 - 3小时以及24小时测量血流量。在对照非缺血期，中枢神经系统所有区域的血流量对24至50毫米汞柱之间的动脉血二氧化碳分压变化表现出显著敏感性。全脑缺血12分钟后，当CBF的重要控制变量保持恒定时，脑血管阻力增加，导致局部血流量减少。全脑缺血后1至3小时，动脉血二氧化碳分压变化对脑血流量的影响几乎完全消失。全脑缺血后24小时内，CBF对PCO2变化的敏感性几乎完全恢复，而继发性严重神经功能缺损仍然存在。全脑缺血后的治疗干预旨在改善“无再流”现象并使残余缺血性神经损伤最小化，必须考虑到缺血后早期对正常强效脑血管舒张影响的敏感性显著降低。
