Abstract

Isocapnic progressive hypoxia was produced by rebreathing 8-10% oxygen in replicate tests during quiet and active sleep, in five full-term calves aged 1-8 days. Airflow through a tightly fitting mask was digitized at 50-ms intervals to calculate breath-by-breath ventilation and rate. Using a cuvette oximeter, arterial O2 saturation (SaO2) was recorded continuously. A mass-spectrometer record of end-tidal PO2 and PCO2 confirmed the mask seal and the constancy of PCO2. Sleep state was characterized by EEG, EOG, neck EMG, and behavior. In quiet sleep the ratio of ventilation to its normoxic control (VR) increased linearly as SaO2 fell; reflex arousal occurred at SaO2 84.9 +/- 4.3% (SD) with VR 1.4 +/- 0.39 (SD). In contrast, during active sleep, hypoxemia progressed without any ventilatory response to a very low SaO2; a reflex arousal occurred at SaO2 59.2 +/- 11.0%, often with a ventilatory response developing abruptly just prior to arousal. The slope of the VR/SaO2 regression lines for the overlapping range of SaO2 differed significantly with state in each animal (P < 0.001); the pooled VR values at SaO2 75% were 1.73 +/- 0.15 (SD) and 0.91 +/- 0.18 for quiet and active sleep respectively. The depression of the ventilatory response to hypoxia in active sleep differs from previous reports on adult dogs. The basis for this difference needs to be evaluated in relation to species and age, in particular in relation to both the mechanics of breathing and to chemoreceptor reflexes.

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