首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Brain concentrations of biogenic amine metabolites in acutely treated and ethanol-dependent rats.
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Brain concentrations of biogenic amine metabolites in acutely treated and ethanol-dependent rats.

机译:急性治疗和乙醇依赖大鼠的生物胺代谢产物的脑浓度。

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摘要

1 Mass fragmentography was used to measure whole brain concentrations of some of the major metabolites of tyramine, octopamine, dopamine and noradrenaline in acutely treated and in ethanol-dependent rats. 2 Treatments with ethanol, either acutely or chronically, failed to alter significantly brain concentration of p-hydroxphenylacetic and p-hydroxymandelic acid (metabolites derived from tyramine and octopamine respectively). The effect on catecholamine metabolites was marked and therefore suggests that ethanol is selective in its effect on central metabolism of biogenic amines. 3 Acute ethanol treatment significantly increased brain concentration of homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylglycol (MHPG). Vanilmandelic acid (VMA) was not affected. All four metabolites (HVA, DOPAC, MHPG and VMA) were increased in the brains of rats rendered dependent on ethanol while still intoxicated (blood ethanol levels above 200 mg/dl). In ethanol-dependent rats undergoing ethanol withdrawal syndrome (no ethanol present in blood), the brain concentrations of HVA and DOPAC were normal while those of MHPG and VMA continued to be elevated. 4 From the decline in the concentrations of HVA and DOPAC after 50 mg pargyline/kg in control rats and rats acutely treated with ethanol, it was concluded that ethanol has no effect on the transport of phenolic acids across the blood brain barrier. 5 No reversal in the metabolism of catecholamines from an oxidative to a reductive pathway, analogous to that produced by ethanol in the periphery, could be established in the brain. 6 The increase in catecholamine metabolite concentrations after ethanol treatment, either acute or chronic, were interpreted as manifestations of increases catecholamine turnover.
机译:1质谱碎片法用于测量急性治疗和酒精依赖型大鼠中酪胺,章鱼胺,多巴胺和去甲肾上腺素的一些主要代谢产物的全脑浓度。 2急性或慢性乙醇治疗均不能显着改变对羟基苯乙酸和对羟基扁桃酸(分别来自酪胺和章鱼胺的代谢物)的脑内浓度。对儿茶酚胺代谢产物的作用是明显的,因此表明乙醇对生物胺的中枢代谢具有选择性。 3急性乙醇治疗显着增加了高香草酸(HVA),3,4-二羟基苯基乙酸(DOPAC)和3-甲氧基-4-羟基苯基乙二醇(MHPG)的脑浓度。香扁桃酸(VMA)不受影响。在仍然依赖酒精(血液中乙醇含量高于200 mg / dl)的情况下,依赖乙醇的大鼠大脑中所有四种代谢物(HVA,DOPAC,MHPG和VMA)均增加。在经历乙醇戒断综合征(血液中无乙醇)的乙醇依赖性大鼠中,HVA和DOPAC的大脑浓度正常,而MHPG和VMA的大脑浓度继续升高。 4从对照大鼠和急性接受乙醇的大鼠中,每公斤50 mg的Pargyline引起的HVA和DOPAC浓度的下降,可以得出结论,乙醇对酚酸跨血脑屏障的转运没有影响。 5在大脑中,无法确定儿茶酚胺的代谢从氧化途径到还原途径的逆转,类似于乙醇在周围产生的逆转。 6乙醇处理后,无论是急性还是慢性的儿茶酚胺代谢物浓度的增加均被解释为儿茶酚胺更新率增加的表现。

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