ABSTRACT
The effect of chronic maternal hypoxia on substance-P immunoreactivity (SPI) was examined in brainstem regions of fetal (gestational day E-28), neonatal (postnatal days 3, 7, 14, 21), and adult rabbits. Time-dated pregnant rabbit does were housed in environmental chambers at gestational day E-10. Between E-14 and E-28, the pregnant does were separated into two groups. Group 1, the control group, breathed 21% O2/79% N2 and group 2 the hypoxia-exposed group, breathed 12-14% O2/86-88% N2. Sacrifice occurred at various days depending on the experimental paradigm. On gestational day E-28, 6 pregnant animals were delivered by hysterotomy and the pups were immediately sacrificed. On and after gestational day E-28, the remaining 12 pregnant animals breathed room air. These animals delivered spontaneously between E-30 and E-32 and the pups remained with their mothers until sacrifice. On postnatal days 3, 7, 14, and 21, SPI was measured by radioimmunoassay in the colliculi (fetal animals), superior and inferior colliculi (postnatal analysis), pons and medulla (both groups). In both prenatally normoxia- and hypoxia-exposed animals, SPI was highest in the medulla, intermediate in the pons and lowest in the colliculi. SPI increased with development. Chronic maternal hypoxia did not alter the caudal-rostral profile nor did it alter the maturational increase in SPI. However, chronic maternal hypoxia increased SPI in prenatal animals and decreased SPI in postnatal animals at 14 and 21 days of life but not in postnatal 3- and 7-day-old animals. These data support the concept that regional differences exist in basal SPI within the brainstem of fetal and neonatal animals, and that maternal hypoxia has both immediate and long-term effects on brainstem SPI.