Hypoxia and ion activities within the brain stem of newborn rabbits.

Eleven rabbits between the 1st and 28th days of life were anesthetized (ketamine 40 mg/kg and acepromazine 3 mg/kg im) thoracotomized, paralyzed, and artificially ventilated with 50% O2 and 10% O2 in N2 or 100% N2. Three-barreled ion-sensitive microelectrodes were used to measure direct-current potentials, potassium (aK+o) and calcium (aCa2+o) activities, and tissue PO2. During control, mean levels of aK+o and aCa2+o were 4.4 +/- 1.1 and 1.3 +/- 0.3 mM, respectively. During hypoxia, changes in aCa2+o were inconsistent, and aK+o revealed three phases: slow (phase I) and fast (phase II) rate of rise and a saturation level (phase III) at the group mean of 6.8 +/- 2.3 mM. Durations of phases I and II decreased, and their slopes increased with maturation. Hypoxia-related excitation of phrenic nerve activity (PHR) occurred during phase I, and gasplike PHR and/or apnea occurred during phases II and III. During recovery after hypoxia, PHR was independent of aK+o levels. Vagal nerve stimulation caused a rapid increase in aK+o followed by a continuous decay even though stimulation continued. Hypoxia had no significant effect on maximal aK+o increase. We concluded that ion homeostasis is less sensitive to the reduced availability of O2 shortly after birth than it is later in life. This age dependence may have an important role in the high resistance to lack of O2 during the early postnatal period in mammals.