[Assessment of the reflex vagal origin of broncho-constrictor effects of hypercapnia in cats (author's transl)].
Breath-by-breath measurements of pulmonary resistance (RL) were used to study the bronchomotor effects produced by the inhalation of a CO2-enriched gas mixture in anaesthetized, spontaneously breathing cats. A significant increase in RL occurred from the second inhalation of the hypercapnic gas mixture. This bronchoconstrictor effect lasted about 18 seconds, then a marked decrease in RL was observed. The secondary bronchodilatation persisted during the entire hypercapnic test (4 min). After surgical suppression of the sensory vagal component at the level of the nodose ganglion (bilateral sensory vagotomy), the early bronchoconstrictor effect of CO2 disappeared, but the secondary bronchodilatation was unchanged. In other experiments, after procaine block of the nervous conduction in non-myelinated vagal fibers, the bronchomotor effects of CO2 were the same as those observed after sensory vagotomy. In contrast, an electrotonic block of both vagus nerves, which abolished nervous conduction in myelinated fibers, did not suppress the bronchoconstrictor response to hypercapnia. Thus, the early increase in RL, which follows inhalation of a hypercapnic gas mixture, seems to be reflexly mediated by vagal afferents, especially by non-myelinated fibers.