II. Effect of CO 2 on afferent vagal endings in the canine lung

Abstract

We have attempted to identify the afferent endings responsible for the pulmonary-CO 2 ventilatory reflex. We recorded afferent vagal impulses arising from the left lung in anesthetized dogs with separately ventilated lungs. When the left pulmonary artery was occluded, left lung P CO 2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung P CO 2 was raised in steps by administration of CO 2, firing decreasing most between 2 and 19 mm Hg, and least between 30 and 50 mm Hg. Irritant receptor activity also increased (from 2.8 to 7.4 impulses/sec) after pulmonary arterial occlusion, the effect being reversed by administration of CO 2. These procedures caused trivial changes in pulmonary and bronchial C-fiber activity. Effects on both slowly-adapting stretch receptors and irritant receptors appeared to result from a direct action of CO 2 on the endings themselves, rather than from mechanical changes in the lung. Changes in slowly-adapting stretch receptor activity provide an adequate explanation for the pulmonary CO 2 ventilatory reflex, the relationship between impulse frequency and lung P CO 2 suggesting that these afferents may have a role in limiting CO 2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.