Phrenic afferent stimulation by bradykinin and the distribution of the inspiratory motor drive.

Activation of thin-fiber (groups III and IV) afferents from the diaphragm using capsaicin or ischemia increases the respiratory muscle activity. To assess whether bradykinin causes similar effects, we injected boluses of bradykinin into the phrenic artery of in situ, isolated and innervated left hemi-diaphragm preparations in 8 alpha-chloralose anesthetized, vagotomized, mechanically ventilated dogs. Inspiratory motor drive during spontaneous breathing attempts was assessed from the integrated EMG activity of several inspiratory muscles. Fifty micrograms of bradykinin increased peak integrated EMG activities of alae nasi to 110%, genioglossus to 189%, left diaphragm to 115% (P < 0.05) and parasternal to 109% (P < 0.01) of baseline activity 60 sec after the injection. Inspiratory time decreased by 10% (P < 0.01). The mean arterial blood pressure increased by about 10 mmHg. Responses were similar with 10, 25 and 100 micrograms of bradykinin. After left phrenicotomy, bradykinin did not affect inspiratory muscle EMG or respiratory timing. In conclusion, thin-fiber phrenic afferent activation by bradykinin exerts an excitatory but disproportionate influence on the inspiratory motor drive.