MODULATION OF MAXIMAL INSPIRATORY AIR-FLOW BY NEUROMUSCULAR ACTIVITY - EFFECT OF CO2

To determine how maximal inspiratory airflow (VI(max)) is modulated by changes in airway neuromuscular activity, we analyzed pressure-flow r elationships obtained during inspiration and expiration in isolated up per airways of anesthetized hyperoxic dogs at different levels of CO2. Inspiratory airflow (VI), hypopharyngeal pressure (Php), pharyngeal p ressure at the flow-limiting site (FLS), and alae nasi (AN) and geniog lossus (GG) electromyographic (EMG) activity were recorded while VI li mitation was produced by rapidly lowering Php until VI plateaued at VI (max). VI(max) and its mechanical determinants, pharyngeal critical pr essure (Pcrit) and nasal resistance (Rn) upstream to the FLS, were mea sured. During hypercapnia (high CO2), VI(max) increased significantly during inspiration (217.3) and expiration (184.1%). These increases we re associated with significant increases in phasic but not tonic AN an d GG activity. They were also associated with decreases in Pcrit from -6.2 +/- 1.6 (SE) at hypocapnia to -9.3 +/- 3.0 and -11.8 +/- 3.4 cmH2 O at high CO2 during expiration and inspiration, respectively. No sign ificant changes in Rn occurred. When phasic neuromuscular activity was abolished by complete neuromuscular blockade in three dogs, these inc reases in VI(max) and decreases in Pcrit at high CO2 were eliminated. When phasic EMG activity was accentuated in four vagotomized dogs, sig nificant increases in VI(max) and decreases in Pcrit were demonstrated during inspiration vs. expiration at high CO2. These findings indicat e that upper airway neuromuscular activity increases VI(max) in the is olated upper airway by decreasing collapsibility (Pcrit) at the FLS si te when neuromuscular activity is stimulated by hypercapnia.