• The Korean Journal of Physiology
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• v.27 no.1
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• pp.37-49
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• 1993

Ventilatory responses to inhaled $CO_2$ were measured during continuous negative pressure breathing (CNPB) in awake dogs. End expiratory lung volume (EELV) decreased linearly with pressure level during CNPB (correlation coefficient= 0.81, p<0.005) during air breathing. When CNPB was applied during 5% $CO_2$ inhalation, the decrease in EELV was not significantly different (p<0.5) from that during air breathing. As a result of a lowered EELV, tidal volume ($V_T$) significantly decreased by 22% and breathing frequency ($f_B$) increased by 68% in the steady state during air breathing (p<0.0001). These responses were similar during 5% $CO_2$ inhalation, thus the $CO_2$ response curve measured during CNPB shifted upward without a change in sensitivity (p>0.05). These results indicate additive effects of CNPB and $CO_2$ inhalation. The degree of hyperventilation during CNPB at eupnea was estimated to be 63% of that during control ventilation and was significantly greater than zero (p<0.0001), which suggests an alveolar hyperventilation due to CNPB. These results suggest that the mechanical alterations associated with n decrease in lung volume could play an important role in ventilatory control independently of chemical regulation of breathing. Thus, exercise hyperpnea, which is associated with a lowered functional residual capacity (FRC), may in part be explained by this mechanical stimulation of breathing.