VENTILATORY AND AROUSAL RESPONSES TO HYPOXIA AND HYPERCAPNIA IN A CANINE MODEL OF OBSTRUCTIVE SLEEP-APNEA

We have previously described a canine model of obstructive sleep apnea (OSA) in which sleep-wake state is monitored continuously by a comput er that produces tracheal occlusion when sleep occurs. Our aim was to assess the effects of long-term application of this model on resting v entilation and on the ventilatory and arousal responses to hypercapnia and hypoxia. Five dogs were maintained on the model for 15.5 +/- 1.7 (mean +/- SE) wk, with a mean apnea index of 57.5 +/- 4.5 occlusions/h of sleep. Resting ventilation and the ventilatory and arousal respons es to progressive hypoxic and hypercapnic rebreathing were assessed du ring wakefulness (W) and both slow-wave (SWS) and rapid-eye-movement ( REM) sleep at baseline prior to intervention, at the end of the OSA ph ase, and following a 1 to 3-mo recovery period. During the period of O SA there were small changes in respiratory timing at rest, but no sign ificant changes in P-CO2 or Sa(O2). As compared with baseline, the ven tilatory response to hypoxia during OSA was strikingly reduced during W, and significantly although less markedly reduced during SWS and REM . The reduction was due to a decreased breathing frequency response to hypoxia. In addition, during OSA there was a significant decrease fro m baseline in Sa(O2) at arousal during hypoxic rebreathing in both SWS and REM. All responses returned to normal during recovery. In contras t to hypoxia, hypercapnic ventilatory responses during OSA were slight ly increased over their baseline values both in W and SWS, owing to a leftward shift of the ventilation-versus-P-CO2 relationship. During re covery, these responses reverted partly to baseline for W and reverted completely to baseline for SWS. There were no significant changes in arousal P-CO2 during hypercapnic rebreathing in either SWS or REM acro ss the pre-OSA baseline, OSA, and post-OSA recovery periods. We conclu de that long-term application of the OSA model is associated with a se lective, reversible decrease in ventilatory and arousal responses to h ypoxia.