Central and peripheral diaphragmatic fatigue in loaded normal and vagotomized dogs.

Severe inspiratory elastic load terminated by respiratory arrest (RA) was studied in 24 anesthetized dogs (group 1, normal: n = 14; group 2, vagotomized: n = 10). The peripheral and central components of the decrease in diaphragmatic force generation and the events preceding RA were studied. We measured stimulated tetanic transdiaphragmatic pressure (Pdi), single twitch compound action potentials, integrated diaphragmatic electromyographic activity (iEMGdi), respiratory frequency (f), inspiratory time, inspiratory drive, overall diaphragmatic activation, and Pdi single twitch superimposed over peak Pdi. Imposed target pressure was -68.8 +/- 4.37 cmH2O for group 1 and -70.9 +/- 4.19 cmH2O for group 2, and the tension-time index of the diaphragm was the same for both groups (0.22 +/- 0.010). During load, 1) f increased in group 1 from 25.4 +/- 1.33 to 41.3 +/- 4.66 cycles/min, and tachypnea was prevented by vagotomy; 2) twitch occlusion persisted until RA and compound action potentials did not change; 3) iEMGdi and inspiratory drive increased and remained high until RA; 4) overall diaphragmatic activation increased 514 (group 1) and 260% (group 2) and then decreased to 228% of the basal value 10 s before RA in group 1 because of a fall in f; and 5) after RA, Pdi stimulated at 60 Hz fell to 39 (group 1; P < 0.0025) and 51% (group 2; NS with group 1) of the basal value. In summary, 1) peripheral fatigue developed without transmission failure; 2) diaphragmatic activation remained maximal until RA; 3) the fall in f appeared as a preterminal event only in group 1; and 4) vagus nerves are necessary for load-induced tachypnea.