Modulation of respiratory responses to carotid sinus nerve stimulation by brain hypoxia

This study examines the effect of progressive isocapnic CO hypoxemia on respiratory afterdischarge and the phrenic neurogram response to supramaximal carotid sinus nerve (CSN) stimulation. Twelve anesthetized, vagotomized, peripherally chemodenervated, ventilated cats with blood pressure controlled were studied. During isocapnic hypoxemia, the amplitude of the phrenic neurogram was progressively depressed. In contrast, the increase in peak phrenic amplitude produced by CSN stimulation was unchanged, suggesting that the central respiratory response to CSN stimulation is unaffected by progressive hypoxemia. The time constant of respiratory afterdischarge (τ) was calculated from best-fit plots of phrenic amplitude vs. time after cessation of CSN stimulation. Under control conditions the value of τ was 57.7 ± 3 (SE) s (n = 12). During progressive isocapnic hypoxemia, τ decreased as a linear function of arterial O₂ content (Ca(O₂)) such that a 40% reduction of Ca(O₂) resulted in a 48% reduction in τ. This reduction of respiratory afterdischarge may contribute to the genesis of periodic breathing during hypoxia.