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本文研究临床上作为抗组织胺的药物赛庚啶(Cyproheptadine)对实验性缺血性损害的作用。实验:使主动脉闭塞致脊髓缺血,连续观察兔子的神经功能,并在闭塞后18小时和120小时对它们评分。将治疗动物的神经功能与不给予药物、缺血时间相同的对照组动物比较,计算出引起50%动物截瘫所需的缺血时间(ET_(50))。试验药物有赛庚啶、喹(口派)嗪和蟾蜍素。结果:对照组缺血后18小时ET_(50)为28.36±2.28分,在缺血开始前10～15分钟,给予赛庚啶1.0mg/kg,明显延长ET_(50)至39.28±1.41分,缺血后5分钟给予同样剂量,ET_(50)是34.46±4.02分,与对照组无显著差异。当剂量增加到2.0mg/kg时,ET_(50)为40.03±4.55分,有显著改善,动物未显示
This article investigates the clinical role of Cyproheptadine, an antihistamine, in experimental ischemic injury. Experiment: Spinal cord ischemia was induced by occlusion of the aorta, the neurological function of the rabbits was continuously observed and scored 18 hours and 120 hours after occlusion. The neurological function of the treated animals was compared with that of the control animals without medication and with the same ischemic time, and the ischemic time (ET_ (50)) required to cause paraplegia in 50% of the animals was calculated. Test drugs are cyproheptadine (quinta minuzepu) and toadstool. Results: In the control group, ET 50 was 28.36 ± 2.28 at 18 hours after ischemia, and 1.0 mg / kg cyproheptadine 10 to 15 minutes before the start of ischemia significantly prolonged ET 50 to 39.28 ± 1.41, The same dose was given 5 minutes after ischemia, ET 50 was 34.46 ± 4.02 points, no significant difference with the control group. When the dose was increased to 2.0mg / kg, ET 50 (50) was 40.03 ± 4.55 points, a significant improvement, the animals did not show