Evidence from the premature infant and fetal sheep indicates that acute hypoxia can disturb normal mechanisms of respiratory control by inducing irregular breathing and/or apnea. These respiratory effects can last longer than the exposure to hypoxia. Similar disturbances of respiratory control have also been associated with the syndrome of sudden infant death (SID); and we postulate that exposure to an abnormally hypoxic environment in fetal or early neonatal life, if sufficiently severe or prolonged, could contribute to the respiratory control defects associated with SID. The proposed investigation is aimed at testing this possibility using an animal model, namely the young of the Virginia opossum (didelphis virginiana). Since the opossum is a marsupial mammal, the young are born at a fetal stage of development. Despite their extreme prematurity, these newborns must breathe the ambient air in a puch on the mother's abdominal wall. It is possible, therefore, to temporarily expose the fetal stage opossum to hypoxia by flushing hypoxic gases through the pouch. Regulation of breathing will be examined plethysmographically in the hypoxia-exposed opossum during subsequent development, and the results will be compared to developmental effects in normal controls. Specifically, breathing pattern, relationships between minute ventilation and oxygen consumption, chemical control of breathing, and pulmonary reflexes are to be investigated. Differences between normal and hypoxia-exposed animals will be analyzed in terms of their possible relationships to events observed in human infants who have succumbed or are at risk to succumb to SID.