Response of medullary respiratory neurons to hypercapnia and isocapnic hypoxia.

Abstract

Single-unit activity was monitored extracellularly from medullary respiratory neurons and nonspecified neurons of decerebrate cats which were paralyzed, vagotomized, and artificially ventilated. Hypercapnia consistently resulted in increased discharge frequencies and decreased modal interspike intervals for respiratory units; peak integrated phrenic discharge heights increased concomitantly. Although isocapnic hypoxia usually resulted in comparable changes, the firing frequency of some respiratory units was depressed. Moreover, this depression was frequently observed simultaneously with a hypoxia-induced increase in phrenic discharge. Nonrespiratory unit discharge was mainly unaltered by hypercapnia or hypoxia. Following bilateral carotid sinus nerve section, hypercapnia-induced increases in respiratory neuronal and phrenic activities were still obtained; hypoxia depressed these activities. It is concluded that central chemoreceptor afferent influences are ubiquitously distributed to the medullary respiratory complex whereas peripheral chemoreceptor afferents produce only a discrete and unequal excitation of respiratory units. Hypoxia-induced ventilatory changes are further concluded to be the net result of peripheral chemoreceptor excitation of respiratory units and a direct depression of the brain stem respiratory complex by hypoxia.