van der Grinten C P, de Vries W R, Luijendijk S C
Department of Pulmonology, University Hospital Maastricht, State University of Limburg, The Netherlands.
Eur J Appl Physiol Occup Physiol. 1991;62(1):49-55. doi: 10.1007/BF00635634.
The vagal amplification of phrenic nerve activity (APHR) was studied as a function of minute ventilation (VE) in 12 spontaneously breathing, anaesthetized cats. Increasing levels of VE were obtained by repeated venous administrations of 2,4-dinitrophenol. The APHR was obtained from the ratio of the phrenic nerve activities in a normal and in an occluded breath. The APHR is thought to be mediated by slowly and/or rapidly adapting stretch receptors. Because airway CO2 may inhibit the discharge of these receptors, we also investigated the influence on APHR of adding 1% and 2% by volume of CO2 to inspired gas. The results showed that an increase in VE had no influence on APHR. The values of APHR ranged from 0.95 to 1.31 and were on average 1.08. Low levels of CO2 in inspired gas did not influence APHR. Our findings suggest that the vagal amplification of central inspiratory output as determined from phrenic nerve activity has a constant gain and it seems to play a relatively unimportant role in sustaining hyperpnoeic breathing.
在12只自主呼吸、麻醉的猫身上，研究了迷走神经对膈神经活动的放大作用（APHR）与分钟通气量（VE）之间的关系。通过反复静脉注射2,4-二硝基苯酚来提高VE水平。APHR通过正常呼吸和屏气时膈神经活动的比值获得。APHR被认为是由慢适应性和/或快适应性牵张感受器介导的。由于气道二氧化碳可能抑制这些感受器的放电，我们还研究了向吸入气体中添加体积分数为1%和2%的二氧化碳对APHR的影响。结果表明，VE增加对APHR没有影响。APHR值在0.95至1.31之间，平均为1.08。吸入气体中低水平的二氧化碳不影响APHR。我们的研究结果表明，根据膈神经活动确定的迷走神经对中枢吸气输出的放大作用具有恒定增益，并且在维持呼吸急促中似乎起相对不重要的作用。
