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目的 :观察氯胺酮对缺血再灌注兔脑血流、CO2 收缩反应性的影响 ,探讨其在脑复苏中的应用价值。方法 :四血管阻断法制作兔全脑缺血 -再灌流模型 ,随机分假手术组、缺血组和氯氨酮组。经颅多普勒超声(TCD)探测大脑中动脉平均血流速度 (Vm) ,过度通气法测定脑血管 CO2 收缩反应。结果 :假手术组脑缺血前 Vm和 CO2 收缩反应性均无显著变化 (P>0 .0 5 )。缺血组再于灌注 2 h、 6h、 2 4 h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假手术组 (P<0 .0 1)。氯胺酮组脑缺血前后 Vm无显著变化 (P>0 .0 5 ) ,但 CO2 反应性明显低于缺血前和同时间点假手术组 (P<0 .0 1)。结论 :氯胺酮可以增加脑缺血再灌注兔脑血流 ,但未能改善其脑血管 CO2 收缩反应性 ,提示氯氨酮可能有一定脑保护作用。
Objective: To observe the effect of ketamine on cerebral blood flow and CO2 contraction reactivity in rabbits with ischemia-reperfusion injury and to explore its value in cerebral resuscitation. Methods: Rabbit model of global cerebral ischemia-reperfusion was established by four-vessel occlusion. The rats were randomly divided into sham operation group, ischemia group and ketamine group. Transcranial Doppler ultrasound (TCD) detection of the middle cerebral artery mean blood flow velocity (Vm), hyperventilation of cerebral vascular CO2 response. Results: There was no significant change in Vm and CO2 contractile response in sham operation group before cerebral ischemia (P> 0.05). In the ischemic group, Vm measured at 2 h, 6 h and 24 h after perfusion, and CO2 reactivity in cerebrovascular were significantly lower than those in the sham operation before and at the same time point (P <0.01). There was no significant change of Vm in ketamine group before and after cerebral ischemia (P> 0.05), but the CO2 reactivity was significantly lower than that in the sham operation group before and at the same time point (P <0.01). CONCLUSION: Ketamine can increase cerebral blood flow in rabbits with cerebral ischemia and reperfusion, but failed to improve its cerebral vascular CO2 reactivity, which suggests that ketamine may have certain cerebral protective effect.