Lu H R, Van Reempts J, Haseldonckx M, Borgers M, Janssen P A
Department of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing.
Am J Emerg Med. 1990 Jan;8(1):1-6. doi: 10.1016/0735-6757(90)90284-7.
A rat cardiopulmonary arrest model was used to study the effects of flunarizine on survival and on the development of postischemic brain damage. Ischemia was induced by a combination of hypovolemia and intracardiac injection of a cold potassiumchloride solution. To validate the model; survival rate and histological damage were assessed after ischemic periods ranging from 5 to 20 minutes. A 6-minute cardiac arrest period was withheld for further therapeutic investigations. In one group (n = 12), flunarizine was administered successively in doses of 0.5 mg/kg intravenous at 5 minutes, 10 mg/kg intraperitoneal at 1 hour, and 20 mg/kg orally at 16 and 24 hours after recirculation. The second group (n = 13) received only the vehicle. Flunarizine, although not affecting mortality; significantly reduced the mean number of ischemic neurons in CA1 hippocampus from 83% in the control to 44% in the drug-treated series (P = 0.014). The results are indicative of the usefulness of this cardiac arrest model to study morphologic aspects of cerebral injury. The results obtained with flunarizine show the effectiveness of this drug even when it is administered after a severe ischemic insult such as global complete ischemia.
采用大鼠心肺骤停模型研究氟桂利嗪对生存率及缺血性脑损伤发展的影响。通过低血容量和心内注射冷氯化钾溶液联合诱导缺血。为验证该模型，在5至20分钟的缺血期后评估生存率和组织学损伤。保留6分钟的心脏骤停期用于进一步的治疗研究。在一组（n = 12）中，在再灌注后5分钟静脉注射氟桂利嗪，剂量为0.5 mg/kg，1小时后腹腔注射10 mg/kg，16小时和24小时口服20 mg/kg。第二组（n = 13）仅接受赋形剂。氟桂利嗪虽然不影响死亡率，但显著降低了CA1海马区缺血神经元的平均数量，从对照组的83%降至药物治疗组的44%（P = 0.014）。结果表明该心脏骤停模型对研究脑损伤的形态学方面有用。氟桂利嗪的研究结果表明，即使在严重缺血性损伤如全脑完全缺血后给药，该药物也有效。
