CHRONIC INTERMITTENT HYPOXIA ALTERS VENTILATORY AND METABOLIC RESPONSES TO ACUTE HYPOXIA IN RATS

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 (V_E; 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 V_E/ 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.

from Physiology via xlomafota13 on Inoreader http://ift.tt/24swog3
via IFTTT