儿茶酚胺分泌是否介导缺氧引起的神经活动增加?

D F Donnelly
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引用次数: 20

摘要

颈动脉体血管球细胞分泌儿茶酚胺被认为是缺氧引起的神经活动增加的原因。为了验证这一假设,我们在体外测量了大鼠颈动脉体的组织儿茶酚胺和单纤维神经活动。缺氧(持续1分钟,最低点0托尔)导致儿茶酚胺释放和神经活动迅速增加,这与假设一致,但重复缺氧穿插短休息时间导致儿茶酚胺释放的下降远远大于神经活动。此外,利血平预处理(24 h)几乎消除了儿茶酚胺的释放,但神经反应与未处理的对照组没有差异。这些结果提示儿茶酚胺的分泌并不是大鼠颈动脉体神经活动增加的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Does catecholamine secretion mediate the hypoxia-induced increase in nerve activity?

Catecholamine secretion from carotid body glomus cells is hypothesized to cause the hypoxia-induced increase in nerve activity. To test aspects of this hypothesis, tissue catecholamine and single-fiber nerve activity was measured from rat carotid bodies in vitro. Hypoxia (1-min duration, 0 Torr at nadir) caused a rapid increase in catecholamine release and nerve activity, consistent with the hypothesis, but repetitive hypoxias interspersed with short rest periods resulted in a much greater decline in catecholamine release than nerve activity. Furthermore, pretreatment with reserpine (24 h) nearly abolished catecholamine release, but nerve response was not different than untreated controls. These results suggest that catecholamine secretion is not causal to the increase in nerve activity of rat carotid body.

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