We determined the effects of chronic exposure to intermittent hypoxia (CIH) on chemoreflex control of ventilation in conscious animals. Adult male Sprague-Dawley rats were exposed to CIH (nadir oxygen saturation [SpO2], 75%; 15 events/hour; 10 hours/day) or normoxia (NORM) for 21 days. We assessed the following responses to acute, graded hypoxia before and after exposures: ventilation (VE; barometric plethysmography), V.O2 and V. CO2 (analysis of expired air), heart rate (HR) and SpO2 (pulse oximetry via neck collar). We quantifed hypoxia-induced chemoreceptor sensitivity by calculating the stimulus-response relationship between SpO2 and the ventilatory equivalent for V.CO2 (linear regression). An additional aim was to determine whether CIH causes proliferation of carotid body glomus cells (bromodeoxyuridine). CIH exposure increased the slope of the VE/ V.CO2/SpO2 relationship and caused hyperventilation in normoxia. Bromodeoxyuridine staining was comparable in CIH and NORM. Thus, our CIH paradigm augmented hypoxic chemosensitivity without causing glomus cell proliferation.
- carotid body
- Copyright © 2016, Journal of Applied Physiology