Kiwull-Schöne H, Ward S A, Kiwull P
Pflugers Arch. 1981 Apr;390(1):63-9. doi: 10.1007/BF00582713.
In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
在麻醉兔中，研究了差异性迷走神经冷阻断对高氧期间吸入二氧化碳通气反应的影响。完全失活后，在适度高碳酸血症范围内，通气量（V）与动脉血二氧化碳分压（PaCO2）之间的关系向左移动并略有变陡，但随着高碳酸血症加剧而逐渐变平。对后一种效应（提示迷走神经介导的通气二氧化碳反应性促进作用）进行了进一步研究。将迷走神经差异性冷阻断至一个温度（5-11摄氏度），该温度消除了布雷尔-黑林充气反射（吸气末气管阻塞不再引起呼气持续时间延长，TE），在正常碳酸血症或高碳酸血症显著水平时对V均无影响。只有进一步将迷走神经冷却至0摄氏度时，高碳酸血症期间的通气抑制才会出现，这主要是因为TE未能对高碳酸血症刺激做出缩短反应。结论是，呼气终止机制的完整性对于迷走神经介导的通气促进作用及其二氧化碳反应性的表现至关重要，这在高氧高碳酸血症期间很明显。有人提出肺上皮刺激感受器或肺牵张感受器的紧张性呼气后期活动可能起作用。
