Phrenic afferent activation modulates cardiorespiratory output in the adult rat.

Phrenic afferents project to brainstem areas responsible for cardiorespiratory control and the mid-cervical spinal cord containing the phrenic motor nucleus. Our purpose was to quantify the impact of small and large diameter phrenic afferent activation on phrenic motor output. Anesthetized and ventilated rats received unilateral phrenic nerve stimulation while contralateral phrenic motor output and blood pressure were recorded. Twelve currents of 40Hz inspiratory-triggered stimulation were delivered (20 seconds on, 5 minutes off) to establish current response curves. Stimulation pulse width was varied to preferentially activate large diameter phrenic afferents (narrow pulse width) and recruit small diameter fibers (wide pulse width). Contralateral phrenic amplitude was elevated immediately post-stimulation at currents above 35 µA for wide, and 70 µA for narrow pulse stimulation when compared to animals not receiving stimulation (time controls). Wide pulse width stimulation also increased phrenic burst frequency at currents ≥35 µA, caused a transient decrease in mean arterial blood pressure at currents ≥50 µA, and resulted in a small change in heart rate at 300 µA. Unilateral dorsal rhizotomy attenuated stimulation-induced cardiorespiratory responses, indicating phrenic afferent activation is required. Additional analyses compared phrenic motor amplitude to output before stimulation and showed that episodic activation of phrenic afferents with narrow pulse stimulation can induce short-term plasticity. We conclude that activation of phrenic afferents: 1) enhances contralateral phrenic motor amplitude when large diameter afferents are activated, and 2) when small diameter fibers are recruited the amplitude response is associated with changes in burst frequency and cardiovascular parameters.