Reflex stimulation of renal sympathetic nerve activity and blood pressure in response to apnea
Reflex stimulation of renal sympathetic nerve activity and blood pressure in response to apnea
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DOI：
10.1164/ajrccm.154.6.8970368
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发表时间：
1996-12-01
影响因子：
24.7
通讯作者：
Shirahata, M
中科院分区：
文献类型：
--
作者：
ODonnell, C;Schwartz, AR;Shirahata, M
本研究旨在探讨传入神经在呼吸暂停时肾交感神经活动（SNA）反射调制中的作用。在使用室内空气或100%氧气通气的麻醉、瘫痪猫（n = 7）中诱导持续时间为20、40和60秒的呼吸暂停。在接受室内空气时，在20-、40-和60-s呼吸暂停期间，肾SNA分别增加34.5 +/-4.2%、53.3 +/-6.4%和59.9 +/- 7.2%（p < 0.005）。在20、40和60秒呼吸暂停期间，接受室内空气时，平均动脉压相应增加（p < 0.025），分别为9 +/- 3、30 +/- 9和45 +/- 12 mmHg。100%氧气的作用是在匹配的Pa-co2水平下降低（p < 0.0001）肾SNA对呼吸暂停的反应至少80%，并消除Pa的任何增加。在呼吸暂停后的第一次呼吸期间，肾SNA部分抑制。在呼吸暂停后的第二次和第三次呼吸期间，肾脏SNA显著下降，这与直接记录的颈动脉化学感受器活性的急剧下降相关（n = 2）。呼吸暂停后肾SNA下降的幅度与呼吸暂停后高血压的程度有关。我们的结论是，缺氧化学感受器刺激是产生肾SNA呼吸暂停反应的主要因素，从胸部传入神经和动脉压力感受器的调制输入可能有助于显着抑制肾SNA呼吸暂停后立即。
The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 +/- 4.2%, 53.3 +/- 6.4%, and 59.9 +/- 7.2% of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (Pal of 9 +/- 3, 30 +/- 9, and 45 +/- 12 man Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100% oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, at a matched level of Pa-co2, by at least 80%, and to eliminate any increase in Pa. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid chemoreceptor activity (n = 2). The magnitude of the fall in renal SNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominant factor generating the renal SNA response to apnea, with modulating inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.