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目的 观察全脑缺血 -再灌流兔脑血流及脑血管CO2 收缩反应性变化 ,探讨复苏后过度通气降颅压的临床应用价值。方法 :四血管阻断法制作兔全脑缺血 -再灌流模型 ,随机分对照组和脑缺血组。经颅多普勒超声 (TCD)探测大脑中动脉平均血流速度 (Vm) ,过度通气法测定CO2 诱发的脑血管收缩反应。结果 :缺血组於再灌流 2、 6、 2 4h所测Vm、脑血管CO2 收缩反应性均明显低于缺血前及同时间点对照组 (P <0 0 0 1) ,CO2 收缩反应性以再灌流 2h最低 ,2 4h有所回升。对照组脑缺血前后Vm 及CO2 收缩反应性无显著变化 (P >0 0 5 )。结论 :兔全脑缺血 -再灌流 2～ 2 4h内前脑循环呈低灌注状态 ,脑血管CO2 收缩反应性降低。该结果提示在缺乏脑血流监测的条件下 ,心肺复苏早期常规使用过度通气降颅压有可能加重脑缺血
Objective To observe the changes of cerebral blood flow and cerebrovascular CO2 reactivity after global cerebral ischemia / reperfusion in rabbits, and to explore the clinical value of hyperventilation and intracranial pressure reduction after resuscitation. Methods: Rabbit model of global cerebral ischemia-reperfusion was established by four-vessel occlusion method and randomly divided into control group and cerebral ischemia group. Transcranial Doppler ultrasound (TCD) was used to detect mean arterial blood flow velocity (Vm) and hyperventilation was used to measure CO2-induced cerebrovascular contractile response. Results: The Vm and cerebrovascular CO2 reactivity measured in ischemic group at 2, 6 and 24 h after reperfusion were significantly lower than those before ischemia and at the same time point (P <0.01), CO2 contractile response To reperfusion 2h minimum, 2 4h has picked up. There was no significant change in Vm and CO2 contractility before and after cerebral ischemia in control group (P> 0.05). CONCLUSION: The forebrain circulation is in a state of hypoperfusion during cerebral ischemia-reperfusion in rabbits and the response to cerebrovascular CO2 is decreased. The results suggest that in the absence of cerebral blood flow monitoring, conventional use of hyperventilation during early CPR reduces intracranial pressure and may aggravate cerebral ischemia