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首页> 外文期刊>Medical Gas Research >Effect of an hyperbaric nitrogen narcotic ambience on arginine and citrulline levels, the precursor and co-product of nitric oxide, in rat striatum
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Effect of an hyperbaric nitrogen narcotic ambience on arginine and citrulline levels, the precursor and co-product of nitric oxide, in rat striatum

机译：高压氮麻醉气氛对大鼠纹状体精氨酸和瓜氨酸水平，一氧化氮的前体和副产物的影响

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Previous studies performed in the laboratory have shown that nitrogen narcosis induces a decrease in striatal glutamate and dopamine levels. Although we stimulated the N-methyl-D-aspartate (NMDA) receptor, an important glutamate receptor required for motor and locomotor activity managed by the striatum, and demonstrated that the receptor was effective when exposed to nitrogen at 3MPa, it was not possible to return the striatal glutamate level to its base values. We conclude that it was the striatopetal neurons of the glutamatergic pathways that were mainly affected in this hyperbaric syndrome, without understanding the principal reasons. Hence we sought to establish what happens in the vicinity of the plasma membrane, downstream the NMDA-Receptor, and we used the hypothesis that there could be neuronal nitric oxide synthase (nNOS) disturbances. A microdialysis study was performed in rat striatum in order to analyse levels of citrulline, the NO co-product, and arginine, the NO precursor. Those both NO metabolites were detectable with an HPLC coupled to a fluorimetric detector. Exposure to pressurized nitrogen induced a reduction in citrulline (-18.9%) and arginine (-10.4%) levels. Under the control normobaric conditions, the striatal NMDA infusion enhanced the citrulline level (+85.6%), whereas under 3 MPa of nitrogen, the same NMDA infusion did not change the citrulline level which remains equivalent to that of the baseline. The level of arginine increased (+45.7%) under normobaric conditions but a decrease occurred in pressurized nitrogen (-51.6%). Retrodialysis with Saclofen and KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of citrulline (+30.5%) and a decrease in arginine levels (-67.4%). There was no significant difference when nitrogen at 3MPa was added. To conclude, the synthesis of citrulline/NO is reduced in nitrogen narcosis while it seems possible to activate it artificially by infusion. We have suggested that the low glutamate levels recorded in nitrogen narcosis induced these dopamine and NO reductions in the striatum.
机译：实验室中进行的先前研究表明，氮麻醉可导致纹状体谷氨酸和多巴胺水平降低。尽管我们通过纹状体刺激了N-甲基-D-天冬氨酸（NMDA）受体（NMDA受体），该受体是运动和运动活动所必需的重要谷氨酸受体，并证明了该受体在3MPa的氮气中有效，但不可能将纹状体谷氨酸水平恢复至基本值。我们得出的结论是，在这种高压综合征中，主要影响的是谷氨酸能途径的纹状体神经元，而不了解其主要原因。因此，我们试图确定在NMDA受体下游的质膜附近发生了什么，并且我们使用了可能存在神经元一氧化氮合酶（nNOS）干扰的假设。在大鼠纹状体中进行了微透析研究，以分析瓜氨酸（NO副产物）和精氨酸（NO前体）的水平。那些两个NO代谢物都可以通过与荧光检测器耦合的HPLC进行检测。暴露于加压氮导致瓜氨酸（-18.9％）和精氨酸（-10.4％）水平降低。在控制的常压条件下，纹状体NMDA输注提高了瓜氨酸水平（+ 85.6％），而在3 MPa的氮气下，相同的NMDA输注不会改变瓜氨酸水平，而瓜氨酸水平仍与基线相当。在常压条件下，精氨酸含量增加（+ 45.7％），但加压氮含量下降（-51.6％）。在常压条件下，在前额叶皮层中使用Saclofen和KCl进行逆透析会导致瓜氨酸的纹状体水平增加（+ 30.5％），精氨酸水平降低（-67.4％）。当添加3MPa的氮气时，没有显着差异。总之，瓜氨酸/ NO的合成在氮麻醉中减少，而似乎可以通过输注人工激活。我们建议氮麻醉中记录的低谷氨酸水平引起纹状体中这些多巴胺和NO的减少。

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