Firing profile of diaphragm single motor unit during hypercapnia and airway occlusion.

To define interaction between chemical and vagal-volume feedback we recorded diaphragm single motor unit (SMU) potentials, tracheal pressure, and end-tidal CO2 in spontaneously breathing, anesthetized cats during hypercapnia and during airway occlusion at functional residual capacity (FRC) or end-inspiratory level (EIL) before and after vagotomy. Hypercapnia increased onset, mean, and peak firing frequencies of early-onset SMUs, caused no change in number of spikes per breath (NSPB), and decreased inspiratory burst duration (Tdi). Airway occlusion increased both NSPB and Tdi without changing onset or mean frequencies. NSPB and Tdi increased more during FRC occlusion than during EIL occlusion. Vagotomy caused effects similar to airway occlusion, except that onset frequency decreased. Increases in NSPB or Tdi following vagotomy were greater than those during FRC occlusion. After vagotomy, airway occlusion no longer altered SMU activity, but hypercapnia still increased onset, mean, and peak frequencies, caused no change in NSPB, and decreased Tdi. New findings in this study are 1) the constancy in NSPB of diaphragm SMUs in response to hypercapnia and 2) the decrease in the onset frequency after vagotomy.