首页> 外文期刊>Brain research bulletin >Nitric oxide synthase expression in the medullary respiratory related nuclei and its involvement in CO-mediated central respiratory effects in neonatal rats.
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Nitric oxide synthase expression in the medullary respiratory related nuclei and its involvement in CO-mediated central respiratory effects in neonatal rats.

机译:一氧化氮合酶在髓样呼吸相关核中的表达及其参与新生大鼠CO介导的中枢呼吸作用的作用。

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The present study was conducted in order to observe the potential participation of the nitric oxide synthase-NO pathway in CO-mediated regulation of respiration of neonatal rats. An immunofluorescent histochemical technique was used to examine the existence of the neuronal nitric oxide synthase, a key enzyme of synthesizing NO, in medullary respiratory nuclei. The rhythmic respiratory-like discharges of hypoglossal rootlets of medullary slices were recorded to test the role of the nitric oxide synthase in CO-mediated respiratory effects. We observed neuronal nitric oxide synthase expressed in the medullary respiratory nuclei in conjunction with CO lengthened expiratory duration, decreased respiratory frequency, and increased inspiratory amplitude. These CO-mediated respiratory effects could be partially eliminated by prior treatment of the slices with Nomega-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase. The results suggest that nitric oxide synthase-NO pathway might be involved in the CO-mediated central regulation of respiration at the level of medulla oblongata in neonatal rats.
机译:进行本研究是为了观察一氧化氮合酶-NO途径在CO介导的新生大鼠呼吸调节中的潜在参与。免疫荧光组织化学技术被用来检查神经元一氧化氮合酶(一种合成NO的关键酶)在髓质呼吸核中的存在。记录了髓质片的舌下根的节律性呼吸样放电,以测试一氧化氮合酶在CO介导的呼吸作用中的作用。我们观察到髓质呼吸核中表达的神经元一氧化氮合酶与CO延长了呼气持续时间,降低了呼吸频率并增加了吸气幅度。通过用Nomega-硝基-L-精氨酸甲酯(一氧化氮合酶的抑制剂)预先处理切片,可以部分消除这些CO介导的呼吸作用。结果表明一氧化氮合酶-NO通路可能参与了新生大鼠长圆形延髓水平下​​CO介导的呼吸中枢调节。

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