title: II. Effect of CO2 on afferent vagal endings in the canine lung.
abstract: We have attempted to identify the afferent endings responsible for the pulmonary-CO2 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 PCO2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung PCO2 was raised in steps by administration of CO2, 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 CO2. 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 CO2 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-CO2 ventilatory reflex, the relationship between impulse frequency and lung PCO2 suggesting that these afferents may have a role in limiting CO2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.
mesh_terms: D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D002245:Carbon Dioxide; D004285:Dogs; D008168:Lung / Q000294:innervation*; D009411:Nerve Endings / Q000502:physiology*; D011652:Pulmonary Circulation; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D012018:Reflex / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology*
chemical_list: D002245:Carbon Dioxide