Edmonds H L, Wauquier A, Melis W, Van den Broeck W A, Van Loon J, Janssen P A
Am J Emerg Med. 1985 Mar;3(2):150-5. doi: 10.1016/0735-6757(85)90040-3.
A 10-minute cardiac arrest was produced in dogs by electrical fibrillation of the heart. Recovery of cerebral function was monitored by estimating the cerebral metabolic rate of oxygen consumption (CMRO2), cerebral blood flow (CBF), electroencephalograph (EEG) and extent of neurological deficit. The study group received flunarizine (0.1 mg/kg intravenously) at the beginning of resuscitation, while control animals were given the drug vehicle. By four hours after resuscitation, CMRO2 in flunarizine-treated dogs was 121 +/- 43% of pre-arrest baseline, as compared with 37 +/- 9% in control animals (P less than 0.02). In the flunarizine group, CBF was 83 +/- 21% of baseline, while it was only 31 +/- 8% in controls (P less than 0.01). As compared with the control group, no other significant changes were detected in electrocardiographic, hemodynamic, or biochemical parameters in the flunarizine-treated dogs. A significant improvement in the visual EEG score (P less than 0.001) and neurological deficit (P less than 0.05) was seen in flunarizine-treated dogs six hours after ischemic insult.
通过心脏电除颤使犬发生10分钟心脏骤停。通过评估脑氧代谢率（CMRO2）、脑血流量（CBF）、脑电图（EEG）和神经功能缺损程度来监测脑功能的恢复情况。研究组在复苏开始时静脉注射氟桂利嗪（0.1mg/kg），而对照组动物给予溶媒。复苏后4小时，氟桂利嗪治疗组犬的CMRO2为心脏骤停前基线的121±43%，而对照组动物为37±9%（P<0.02）。在氟桂利嗪组，CBF为基线的83±21%，而对照组仅为31±8%（P<0.01）。与对照组相比，氟桂利嗪治疗组犬的心电图、血流动力学或生化参数未检测到其他显著变化。缺血性损伤6小时后，氟桂利嗪治疗组犬的视觉EEG评分（P<0.001）和神经功能缺损（P<0.05）有显著改善。
