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目的:以血浆3,4-二羟苯乙醇(DHPG)和3,4-二羟苯乙酸(DOMA)的变化为判断指标,研究去甲肾上腺素(NE)在神经元内的代谢.方法:大鼠去脊髓并给予2.5Hz电刺激合并静脉内输入NE(6 nmol·kg~(-1)·min~(-1)).同位素酶标法测定血浆DHPG和DOMA浓度.结果:当静脉内输入NE使血浆NE浓度增加了100倍时,血浆DHPG和DOMA分别增加了12倍和1.2倍.地昔帕明(2mg/kg iv)使血浆DHPG浓度降低为对照组的25％,而DOMA无明显变化.MAO-A抑制剂氯吉林使血浆DHPG和DOMA浓度分别降低为对照组的15％和70％,MAO-B抑制剂司立吉林使二者的血浆浓度分别降低为对照组的26％和76％.氯吉林与司立吉林合用使血浆DHPG几乎完全消失,而DOMA无明显变化.结论:去甲肾上腺素被突触前膜摄取后,经线粒体外膜上的MAO氧化脱胺、还原产生DHPG为其主要代谢途径.
Objective: To study the metabolism of norepinephrine (NE) in neurons using the changes of plasma 3,4-dihydroxyphenyl ethanol (DHPG) and 3,4-dihydroxyphenylacetic acid (DOMA) as indexes.Methods: The rats were sacrificed and the spinal cord was obtained and stimulated with 2.5 Hz electrical stimulation (6 nmol · kg -1 · min -1) intravenously.The concentrations of plasma DHPG and DOMA were measured by isotope enzyme labeling.Results: Plasma DHPG and DOMA increased by 12-fold and 1.2-fold, respectively, with addition of NE at a 100-fold increase in plasma NE concentration. Desipramine (2 mg / kg iv) reduced plasma DHPG concentration to 25% of the control group, while DOMA-free The MAO-A inhibitor clindamycin reduced plasma concentrations of DHPG and DOMA to 15% and 70% of the control group, respectively, while MAO-B inhibitor and clindamycin reduced the plasma concentrations of both to 26% And 76%, respectively.The combination of clindamipine and selegiline resulted in the almost complete disappearance of plasma DHPG, but no significant changes in DOMA.Conclusion: Norepinephrine is up-regulated by the pre-synaptic membrane and oxidized and deaminated by MAO on the mitochondrial outer membrane Produce DHPG as its main metabolic pathway.