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麦角隐亭对缺血性脑损伤的影响。

Effect of mergocriptine on postischemic brain damages.

作者信息

Nagasawa H, Izumiyama K, Kogure K

机构信息

Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Arzneimittelforschung. 1991 Nov;41(11):1119-22.

PMID:1810256
Abstract

The effects of mergocriptine (2-methyl-a-ergocryptine; CBM36-733; CAS 81968-16-3) on ischemia-induced brain damages were studied using both a global and a focal ischemia model. First, immediately after 5 min of forebrain ischemia induced by ligation of the bilateral carotid arteries of Mongolian gerbils, the animals were intraperitoneally injected with 3 mg/kg or 10 mg/kg CBM36-733. Seven days after ischemia, perfusion-fixed brains were processed by conventional histology. The number of neurons per mm in the CA 1 pyramidal cell layer was calculated and they were labelled neuronal density. In the control group, the neuronal density was 69.7 +/- 7.2 (mean +/- SEM/mm), in the vehicle group and 3 mg/kg of CBM36-733 treated group, they were 12.2 +/- 4.4 and 11.6 +/- 5.1, respectively. The neuronal density in the 10 mg/kg of CBM36-733 treated group was 42.2 +/- 8.4. These data indicate that 10 mg/kg of CBM36-733 protects on the CA 1 neurons against ischemia induced delayed neuronal death. Second, the effect of long-term administration of 3 mg/kg CBM36-733 on focal brain ischemia of the rats was studied by measuring regional cerebral blood flow and glucose metabolism by autoradiograms. After 90 min of middle cerebral artery occlusion, the rats were intraperitoneally injected with 3 mg/kg of CBM36-733 every day for 2 weeks. There were no significant differences in cerebral blood flow and glucose metabolism between the treated group and the vehicle group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

使用全脑缺血模型和局灶性缺血模型,研究了麦角隐亭(2-甲基-α-麦角隐亭;CBM36-733;CAS 81968-16-3)对缺血性脑损伤的影响。首先,在结扎蒙古沙土鼠双侧颈动脉诱导前脑缺血5分钟后,立即给动物腹腔注射3毫克/千克或10毫克/千克的CBM36-733。缺血7天后,对灌注固定的大脑进行常规组织学处理。计算CA1锥体细胞层每毫米的神经元数量,并将其标记为神经元密度。对照组的神经元密度为69.7±7.2(平均值±标准误/毫米),溶剂对照组和3毫克/千克CBM36-733治疗组的神经元密度分别为12.2±4.4和11.6±5.1。10毫克/千克CBM36-733治疗组的神经元密度为42.2±8.4。这些数据表明,10毫克/千克的CBM36-733可保护CA1神经元免受缺血诱导的迟发性神经元死亡。其次,通过放射自显影测量局部脑血流量和葡萄糖代谢,研究了长期给予3毫克/千克CBM36-733对大鼠局灶性脑缺血的影响。大脑中动脉闭塞90分钟后,大鼠每天腹腔注射3毫克/千克的CBM36-733,持续2周。治疗组和溶剂对照组之间的脑血流量和葡萄糖代谢没有显著差异。(摘要截取自250字)

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