Chronic intermittent hypoxia exposure for 21 days augmented hypoxic chemosensitivity and caused hyperventilation in normoxia without causing glomus cell proliferation in rats.
Chronic intermittent hypoxia in rats augments hypoxic chemosensitivity without causing glomus cell proliferation.
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/h; 10 h/day or normoxia (NORM) for 21 days. We assessed the following responses to acute, graded hypoxia before and after exposures: ventilation (V̇e, via barometric plethysmography), V̇o2 and V̇co2 (analysis of expired air), heart rate (HR), and SpO2 (pulse oximetry via neck collar). We quantified hypoxia-induced chemoreceptor sensitivity by calculating the stimulus-response relationship between SpO2 and the ventilatory equivalent for V̇co2 (linear regression). An additional aim was to determine whether CIH causes proliferation of carotid body glomus cells (using bromodeoxyuridine). CIH exposure increased the slope of the V̇e/V̇co2/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.
Morgan et al. (2016) studied Chronic intermittent hypoxia. Chronic exposure to intermittent hypoxia (CIH) vs. Normoxia (NORM) was evaluated on Hypoxia-induced chemoreceptor sensitivity (slope of the V̇e/V̇co2/SpO2 relationship). Chronic intermittent hypoxia exposure for 21 days augmented hypoxic chemosensitivity and caused hyperventilation in normoxia without causing glomus cell proliferation in rats.