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动脉及心肺压力感受器和化学感受器对兔耳交感神经放电的影响及相互作用。

Arterial and cardiopulmonary baroreceptor and chemoreceptor influences and interactions on ear sympathetic nerve discharge in the rabbit.

作者信息

Iriki M, Kozawa E, Korner P I, Dorward P K

出版信息

Jpn J Physiol. 1979;29(5):551-8. doi: 10.2170/jjphysiol.29.551.

Abstract
  1. The effects of changing intravascular pressures on integrated ear sympathetic nerve activity (ESNA) were studied in anesthetized artificially ventilated rabbits by inflating aortic and inferior vena caval perivascular balloons under conditions of normal arterial Po2 and during arterial hypoxia. 2. At normal Po2 ESNA was unaffected by arterial and cardiopulmonary baroreflex influences. The small inhibition of ESNA observed during rises in arterial pressure after vagotomy was also present after section of the carotid sinus and aortic nerves, and after cutting both vagi as well. 3. During hypoxia there was marked inhibition of ESNA, which was minimally influenced by vagotomy but abolished by section of the carotid sinus and aortic nerves, suggesting that it was chemoreceptor-mediated. There was a pressure-related rise in ESNA which was abolished by vagotomy and considered to be due to a central nervous chemoreceptor-cardiopulmonary baroreflex interaction.
摘要
  1. 在麻醉的人工通气兔中,通过在正常动脉血氧分压条件下以及动脉缺氧期间向主动脉和下腔静脉血管周围气囊充气,研究了血管内压力变化对耳交感神经综合活动(ESNA)的影响。2. 在正常血氧分压时,ESNA不受动脉和心肺压力反射影响。迷走神经切断术后动脉压升高时观察到的ESNA轻度抑制,在切断颈动脉窦和主动脉神经后以及双侧迷走神经切断后也存在。3. 在缺氧期间,ESNA受到显著抑制,迷走神经切断对其影响极小,但颈动脉窦和主动脉神经切断后则消除了这种抑制,提示这是化学感受器介导的。ESNA存在与压力相关的升高,迷走神经切断可消除这种升高,认为这是由于中枢神经化学感受器 - 心肺压力反射相互作用所致。

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