The effects of asphyxia on afferent activity recorded from the cervical vagus in the duck.

Recordings were made of nervous activity from duck arterial chemoreceptors, arterial baroreceptors and pulmonary receptors during steady-state conditions (normoxic normocapnia, hypoxia, and hypercapnia) and apnoeic asphyxia. Arterial chemoreceptors were stimulated by hypoxia and intra-arterial KCN injection and showed an increasing discharge throughout asphyxia. During the first 2 min of asphyxia the time course of the development of asphyxic bradycardia paralleled that of the increase in arterial chemoreceptor discharge. Arterial baroreceptors discharged at a constant latency from the heart beat when mean arterial pressure was constant, while a drug-induced increase in mean arterial pressure was associated with a reduced latency and increased baroreceptor activity per heart-beat. During asphyxia mean arterial pressure often rose so that, despite the effect of bradycardia, baroreceptor activity per heart-beat and activity per unit time increased. Pulmonary receptors showed a linear relationship (negative slope) between discharge rate and % CO2 in inspired air and usually stopped firing in apnoeic asphyxia. The initiation and maintenance of diving bradycardia are discussed in terms of these results.