AIRWAY HYPERREACTIVITY PRODUCED BY SHORT-TERM EXPOSURE TO HYPEROXIA IN NEONATAL GUINEA-PIGS

Airway hyperreactivity is recognized as one of the long-term sequelae of bronchopulmonary dysplasia (BPD). Due to the improved care and prog nosis of very low-birth weight infants, the incidence of BPD is increa sing. There are data that suggest the increased survival of premature infants may be associated with the observed increased incidence of chi ldhood asthma. The hyperoxia received as part of the treatment of resp iratory distress syndrome is believed to be partly if not completely r esponsible for BPD. To gain insight into the potential role that hyper oxia might play in producing airway hyperreactivity, 4-day-old guinea pig pups were exposed to 70% oxygen or air for 96 h, and airway respon siveness to acetylcholine (ACh) was assessed both 2 and 9 days after t he completion of the hyperoxia exposures. Unlike ozone, the mechanism for the persistently increased airway reactivity is not related either to the inhibition of neuronal acetylcholinesterase or inhibition of t he neuronal Mg muscarinic receptor. A difference in antioxidant protec tion did not account for the increased response of the neonatal guinea pigs compared with hyperoxia-exposed rat pups. These data support the usefulness of the neonatal guinea pig as a model to study the mechani sm responsible for hyperoxia-induced airway hyperreactivity.