Fig 2. The cough motor pattern was minimally affected by cough induced hyperventilation (CHV) while the cough-to-eupnea transition remained sensitive to changes in CO₂.

A) Esophageal pressure and end-tidal CO₂ (ETCO₂) recording traces of 60 second cough trials without and with added CO₂ added are shown from a single animal. Cough was stimulated for 60 seconds using a flexible plastic cannula inserted into the tracheostomy tube. In both conditions, an arterial blood gas (ABG) was recorded 45 seconds into the cough trial. During the control condition (top trace), no CO₂ was added. During the isocapnic condition (bottom trace), 10% CO₂ was added to the animal’s inspired gas 10s after the cough stimulus began; the flow was adjusted so that the end-tidal CO₂ matched levels seen during eupnea. B) Apnea duration was sensitive to the presence of cough and to CO₂ level. Recovery data from mechanical hyperventilation, cough-induced hyperventilation, and isocapnic repetitive coughing are shown. Animals were either mechanically hyperventilated to apnea (n = 5), exposed to cough-induced hyperventilation (CHV. n = 12), or to isocapnic cough conditions with added CO₂ (n = 12). Although both mechanical hyperventilation and CHV decrease CO₂, the apneic period after CHV was shorter than that following mechanically-induced hyperventilation. When CO₂ was added (isocapnia), the apnea was even shorter. C) The period of reduced breathing (hypopnea) before returning to eupneic-like breathing was influenced by arterial/end tidal CO₂ (isocapnia) but not affected by cough (CHV). ♦ = p < 0.05 (Mann-Whitney test). ## = p < 0.05 (Wilcoxon singed-rank test). ¤¤ = p < 0.01, ¤ p = < 0.05 (Welch t-test). CHV/Isocapnia n = 12, Ventilator n = 5.