Background: Hypoxia experienced by the fetus is a major cause of disturbed neural and cardiorespiratory function during childhood. This is of importance in pediatric research assuming that the sudden infant death syndrome may be preceeded by chronic hypoxia.

Subjects: The aim of the study was to test whether hypoxia during gestation could subsequently affect the catecholamine turnover in childhood and adulthood with special regard to peripheral chemoreceptors, brain areas involved in cardiorespiratory events and sympathoadrenal system.

Interventions: 20 pregnant Sprague-Dawley rats were maintained under normoxia and 20 pregnant Sprague-Dawley rats were exposed to hypoxia(10% O2) from days 5 to 20 of gestation (E5-E20). Litters were delivered under normoxia and grew up under normoxia until sacrifice. Male normoxic control(n=54) and male gestational hypoxic (n=52) rats were examined at 1, 3 or 8 weeks. The levels and turnover of dopamine (DA) and norepinephrine (NE) were assayed in carotid bodies, noradrenergic cell groups A2, adrenals and heart.

Results: In the carotid bodies of 1-, 3- and 8-weeks old rats exposed to hypoxia during gestation, the levels of DA decreased respectively by 50%, 43% and 36%. In the caudal part of the A2 cell group of the nucleus tractus solitarius, the turnover of NE was almost fully inhibited at 3 weeks of age and was not further altered in the 8-weeks old rats. In the adrenals and heart, the turnover of DA and NE respectively remained significantly reduced (-31% and -74% at 8 weeks).

Conclusion: Gestational hypoxia in rats induces long-term depressive neurochemical changes of most of the catecholaminergic areas involved in the chemoreflex pathways. Although these effects diminished or disappeared with advancing age, they may contribute to alter the cardiorespiratory function in childhood. INSERM CRE 937002, Région Rhône-Alpes, Swedish MRC 05234.