Changes in efferent pulmonary sympathetic nerve activity during systemic hypoxia in anesthetized cats.

Changes in efferent pulmonary sympathetic nerve activity during systemic hypoxia in anesthetized cats.
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麻醉猫全身缺氧期间传出肺交感神经活动的变化。

DOI:
10.1152/ajpregu.1995.269.6.r1404
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发表时间:
1995
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
I. Ninomiya
I. Ninomiya
中科院分区:
--
文献类型:
--
作者:
M. Shirai;K. Matsukawa;N. Nishiura;A. Kawaguchi;I. Ninomiya

文献摘要

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在全身缺氧时,对肺血管的传出交感神经活动的变化尚未阐明。本研究的目的是确定麻醉猫在鼻窦主动脉断神经加迷走神经切开术前后肺交感神经活动(PSNA)对急性全身性缺氧的反应。去神经支配是为了估计中枢神经系统介导的外周化学感受器和压力感受器独立的PSNA变化。从切断的神经束中央端记录PSNA,该神经束与供应膈叶的大叶动脉分离。同时测量肾交感神经活动(RSNA)、全身和肺动脉压。动物接受大约3分钟的分级缺氧(吸入16、12、8、5和3%的氧气)。从常氧降至约45托的动脉血氧分压(PaO2)(吸入12-21%的氧气)时,PSNA没有变化。低于这个水平,PSNA开始增加,并且在PaO2约为15 Torr(含3% O2)时明显增加(约2.5倍)。缺氧时PSNA的升高明显大于RSNA, PaO2小于约30 Torr (3-8% O2)。特别是在PaO2约为15 Torr时,PSNA的增加幅度是RSNA的两倍。去神经支配后,缺氧PSNA升高在PaO2约25 ~约45 Torr(含5-12% O2)时明显减弱,但衰减很小;因此,多数PSNA持续增加。相比之下,缺氧RSNA的增加在去神经支配后大部分被消除。结果表明,全身缺氧对PSNA的神经反射作用明显大于对RSNA的神经反射作用,提示缺氧时PSNA的升高主要由中枢机制介导,而RSNA的升高主要由外周化学感受器引起。
Changes in efferent sympathetic nerve activity to the pulmonary vessels during systemic hypoxia have yet to be elucidated. The purpose of this study was to determine the pulmonary sympathetic nerve activity (PSNA) changes in response to acute systemic hypoxia before and after sinoaortic denervation plus vagotomy in anesthetized cats. The denervation was performed to estimate the central nervous system-mediated peripheral chemoreceptor- and baroreceptor-independent PSNA change. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and systemic and pulmonary arterial pressures were also measured simultaneously. The animals were submitted to approximately 3-min periods of graded hypoxia (16, 12, 8, 5, and 3% O2 inhalations). PSNA did not change from normoxia down to an arterial O2 partial pressure (PaO2) of approximately 45 Torr (with 12-21% O2 inhalations). Below this level, PSNA began to increase, and markedly so (approximately 2.5-fold) at a PaO2 of approximately 15 Torr (with 3% O2). The hypoxic PSNA increase was significantly larger than that for RSNA, with a PaO2 of less than approximately 30 Torr (with 3-8% O2). Particularly at a PaO2 of approximately 15 Torr, the magnitude of the PSNA increase was two times greater than that for RSNA. After denervation, the hypoxic PSNA increase was significantly attenuated at a PaO2 of approximately 25 to approximately 45 Torr (with 5-12% O2), but the attenuation was very small; therefore most of the PSNA increase persisted. The hypoxic RSNA increase, in contrast, was mostly abolished after denervation. The data indicate that the neural reflex effect of systemic hypoxia on PSNA is significantly greater than that on RSNA and suggest that the hypoxic PSNA increase is mostly mediated by central mechanisms, whereas that for RSNA is chiefly caused by peripheral chemoreceptors.