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Newborn infants and animals typically exhibit a paradoxical ventilatory response to hypoxia. The depressive phase of the response has not been adequately explained. It has been suggested that hypoxia may cause the release of inhibitory neuromodulators which depress ventilation. We have postulated that the nucleoside, adenosine, may be involved because 1) it is rapidly released during hypoxia, 2) it depresses ventilation, and 3) theophylline, a competitive inhibitor, has successfully been used to treat apnea of prematurity. Herein we describe the effects of aminophylline on ventilation during hypoxia in the spontaneously breathing newborn piglet administered both rapidly after ventilatory depression has occurred (bolus) and before the onset of hypoxia (pretreatment). Ten percent oxygen breathing produced a typical biphasic ventilatory response. The decrease in minute ventilation was caused by a decrease in both tidal volume and respiratory frequency. The bolus administration of aminophylline reversed the depression in minute ventilation (p < 0.001) by increasing tital volume (p< 0.002). Pretreatment with aminophylline decreased the amount of ventilatory depression (p< 0.05) by preventing a decrease in respiratory frequency. We conclude that aminophylline, an adenosine antagonist, reduces the decrease in ventilation which occurs during hypoxia in the newborn. We speculate that adenosine may play a role in hypoxic ventilatory depression and respiratory control in the newborn.

Alterations in thermoregulatory mechanisms related to sleep state may play an important role in the problems of homeostasis experienced by the premature infant. In the adult, homeothermic regulation of body temperature may be suspended during REM. We measured oxygen consumption (O2) in six premature infants 33–35 wk gestation both at thermoneutrality and during a mild thermal stress to determine whether thermoregulatory responses were intact during REM sleep. All infants were studied under radiant warmers. Skin temperature was allowed to fall 7–8 times during a 6–8 h study period while O2, CO2, heart rate and TcPO2were continuously recorded. Sleep state was scored using EEG, EOG, EMG and behavioral criteria. A total of 1,162 one-min epochs were scored. In all states including REM, O2was significantly higher during the cool periods. The mean increases: 21.5, 23.3, 11.1 and 5.3 for Awake, Indeterminate, REM and NREM respectively. When REM and NREM were compared at thermoneutrality, there was no difference in the O2(8.80 ± 0.11 and 8.93 ± 0.15 cc/kg/min, mean ± S.E., for REM and NREM, respectively). We conclude that in contrast to the adult, active thermoregulation occurs in the premature infant during REM sleep.