稳态常氧状态下颈动脉和主动脉对通气化学感觉驱动和短暂缺氧诱导的通气化学反射的相关贡献。

J Eugenin, C Larraín, P Zapata
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引用次数: 0

摘要

研究了自主呼吸戊巴比妥麻醉的成年猫外周动脉化学感受器对强直性和相性反射通气调节的作用。麻醉阻断缓冲神经所引起的短暂通气效应,推测了高氧缺氧时的化学感觉驱动。主动脉神经阻滞不改变通气。颈动脉神经阻滞引起短暂性通气抑制,VT降低46%,fR降低26%,随后VT、fR和PETCO2恢复到稳态值。PETCO2的变化与VT相关,但与fR无关。当对侧颈动脉神经已经被阻塞时,阻塞给定颈动脉神经的通气作用更强烈。这种效应可能是颈动脉神经输入与通气的化学感觉驱动之间的低加性相互作用的表达。通过对缓冲神经阻断前后NaCN静脉注射引起的通气反射的剂量-反应曲线分析,发现颈动脉神经对高剂量NaCN通气反射的反应起主要作用,主动脉神经对高剂量NaCN通气反应的作用较小。各颈动脉神经对强直性化学感觉驱动和阶段性通气化学反射的贡献高度相关(rs = 0.90;P < 0.01)。我们提出一系列调节功能可以描述外周动脉化学感受器在常氧条件下对强直性通气驱动和低氧条件下引起的相反射反应的影响。颈动脉神经介导的调节在正常缺氧状态下是明显的,而由主动脉神经提供的调节仅在明显缺氧状态下表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Correlative contribution of carotid and aortic afferences to the ventilatory chemosensory drive in steady-state normoxia and to the ventilatory chemoreflexes induced by transient hypoxia.

The contributions of the peripheral arterial chemoreceptors to the tonic and phasic reflex ventilatory regulation were studied in spontaneously breathing pentobarbitone anesthetized adult cats. The chemosensory drive during eucapnic normoxia was inferred from the transient ventilatory effects induced by anesthetic blockade of the buffer nerves. Aortic nerves block did not modify ventilation. Carotid nerves block provoked transient ventilatory depression, decreasing VT by 46% and fR by 26%, followed by recovery to steady-state values in VT, fR and PETCO2. Changes in PETCO2 were correlated with those in VT, but not with those in fR. The ventilatory effects of blocking a given carotid nerve were more intense when the contralateral carotid nerve was already blocked. This effect may be an expression of hypoadditive interactions between carotid nerves inputs with respect to chemosensory drive of ventilation. Analysis of the dose-response curves for the ventilatory reflexes evoked by NaCN i.v., before and after blockade of the buffer nerves, revealed major contributions of the carotid nerves, with small contributions of the aortic nerves to the those responses to high doses of NaCN. The contributions of each carotid nerve to the tonic chemosensory drive and to the phasic ventilatory chemoreflexes were highly correlated (rs = 0.90; p less than 0.01). We propose that a family of modulatory functions may describe the effects exerted by the peripheral arterial chemoreceptors upon the tonic ventilatory drive in normoxia and the phasic reflex responses evoked by hypoxia. While the carotid nerves mediated modulation is evident in normoxia, that provided by both aortic nerves is only expressed during pronounced hypoxia.

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