Environmental Hyperoxia and Development of Carotid Chemoafferent Function
Exposure to hyperoxia in the first few weeks of life causes life-long impairment of carotid chemoreceptor function in rats, e.g., depressed carotid sinus nerve (CSN) and phrenic nerve responses to acute hypoxia. We determined the maximal CSN responses of anesthetized adult rats to severe hypoxia (ventilation with 100% N2) or asphyxia (stopped ventilator) after 1, 2, and 4 weeks of postnatal hyperoxia (60% O2) (PNH). As with acute responses to hypoxic stimuli, we find that maximal CSN responses are significantly attenuated with severity of attenuation dependent on duration of PNH. We suggest that impaired carotid chemoafferent input produced by PNH could play a role in failure of arousal in severely hypoxic states occurring in infants and adults.
KeywordsCarotid Body Bronchopulmonary Dysplasia Acute Hypoxia Moderate Hypoxia Hyperoxic Exposure
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