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[脑缺血小鼠的脑能量代谢及某些药物的作用]

[Brain energy metabolism of cerebral ischemic mice and the effects of some drugs].

作者信息

Feng Y P, Sun Y D, Chen B T, Ye G, Zeng G Y

出版信息

Yao Xue Xue Bao. 1989;24(2):89-94.

PMID:2801143
Abstract

Two simple cerebral ischemic models of mice were used for studying brain energy metabolism and the effects of drugs. Model one is partial occlusion of the left carotid artery and total occlusion of the right one including the vagus. The behavior of the animals appeared splaying of the contralateral extremities, circling around counterclockwise and in a comatose motionless state. Following the designated ischemic time, the animals were put into liquid N2. Model two is decapitation induced ischemia of mouse brain. The whole animal (control) and the severed head were rapidly frozen in liquid nitrogen 0, 10, 30, 60 s after decapitation. Brain samples were powdered at liquid N2 temperature, extracted and determined for ATP, phosphocreatine (Pcr) and lactic acid (LA). The data from model one indicate that after an ischemic period of 10 min, brain LA level increased significantly compared with values from the sham operated group, while no significant alteration was observed in brain ATP, and Pcr level. At 180 min of ischemia, levels of ATP and Pcr were considerably reduced while LA level increased significantly. The degree of symptoms induced by brain ischemia showed good correlation with brain energy metabolism. In model 2 brain LA level was found to be increased, while ATP and Pcr levels decreased after whole brain ischemia. However, brain ATP and Pcr levels were increased and LA level was decreased significantly in the normal and ischemic animal after administration of phenobarbital (225 mg/kg ip). LA level decreased significantly in the unischemic mice treated with Rb1 (100 mg/kg ip). It is indicated that both models of cerebral ischemia were simple and sensitive methods for studying brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

使用两种简单的小鼠脑缺血模型来研究脑能量代谢及药物的作用。模型一是左侧颈动脉部分闭塞,右侧包括迷走神经在内的颈动脉完全闭塞。动物的行为表现为对侧肢体伸展、逆时针转圈以及处于昏迷不动状态。在设定的缺血时间后,将动物放入液氮中。模型二是断头诱导的小鼠脑缺血。在断头后0、10、30、60秒,将整个动物(对照组)和断头迅速在液氮中冷冻。将脑样本在液氮温度下研磨成粉末,提取并测定三磷酸腺苷(ATP)、磷酸肌酸(Pcr)和乳酸(LA)。模型一的数据表明,缺血10分钟后,与假手术组相比,脑LA水平显著升高,而脑ATP和Pcr水平未观察到显著变化。在缺血180分钟时,ATP和Pcr水平大幅降低,而LA水平显著升高。脑缺血诱导的症状程度与脑能量代谢呈现良好的相关性。在模型二中,发现全脑缺血后脑LA水平升高,而ATP和Pcr水平降低。然而,在给予苯巴比妥(225毫克/千克腹腔注射)后,正常和缺血动物的脑ATP和Pcr水平升高,LA水平显著降低。用Rb1(100毫克/千克腹腔注射)处理的未缺血小鼠中LA水平显著降低。表明这两种脑缺血模型都是研究脑缺血的简单且敏感的方法。(摘要截断于250字)

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