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[氧诱导癫痫惊厥前期氧化脱氨基反应的动力学]

[Kinetics of the oxidative deamination reaction in the preconvulsive period of oxygen-induced epilepsy].

作者信息

Gol'dina O A, Gankina E M, Mansil'ia V A, Koloskov Iu B, Demurov E A

出版信息

Biull Eksp Biol Med. 1989 Apr;107(4):417-20.

PMID:2720154
Abstract

Kinetic parameters of monoamine oxidative deamination in compensatory and preconvulsive periods of oxygen epilepsia were studied. It was shown that in rat brain MAO's affinity for serotonin reduced from the 5th minute of exposure to hyperbaric oxygen and went on reducing on the 15th minute. In rat heart the affinity of MAO for serotonin firstly decreased and then returned to normal meaning. Dopamine deamination in rat brain in compensatory period of epilepsia was activated and then was inhibited. In rat heart from the 5th minute of exposure to oxygen dopamine and 2-phenylethylamine deamination was blocked. Tyramine deamination in preconvulsive period of epilepsia changed in a complex manner. It is concluded that the kinetic parameters of monoamine deamination change in the initial phases of exposure to hyperbaric oxygen, and the most distinct modifications take place in rat heart, but not in rat brain.

摘要

研究了氧性癫痫代偿期和惊厥前期单胺氧化脱氨的动力学参数。结果表明,在大鼠脑中,从暴露于高压氧的第5分钟起,单胺氧化酶(MAO)对5-羟色胺的亲和力降低,并在第15分钟继续降低。在大鼠心脏中,MAO对5-羟色胺的亲和力先降低,然后恢复到正常水平。在癫痫代偿期,大鼠脑中多巴胺脱氨被激活,然后受到抑制。从暴露于氧气的第5分钟起,大鼠心脏中多巴胺和2-苯乙胺的脱氨被阻断。癫痫惊厥前期酪胺脱氨以复杂的方式变化。得出的结论是,在暴露于高压氧的初始阶段,单胺脱氨的动力学参数发生变化,最明显的变化发生在大鼠心脏,而不是大鼠脑中。

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