CONICET | Buscador de Institutos y Recursos Humanos

Despite intense research over the years, the complex, but well coordinated mechanisms that control the onset and maintenance of labour remains unrevealed. Previous data regard the capacity of cerebrovascular regulation during asphyxia for prevention of brain oxygen deficit in newborns. We measured nitrite formation (NO2), asymmetric dimethylarginine (ADMA) and nitroso-hemoglobin (NOHb) in the feto-placental circulation of pregnancies concluded with labour and intra-partuum hypoxia and in the peripheral blood of the newborns. We enrolled 35 pregnancies terminated with vaginal delivery, 30 with caesarean section after labour because of unrelated obstetrical problems and 20 concluded by programmed caesarean section because of several indications. We found increased NO2 and NOHb in the umbilical vein of pregnancies concluded with labour. Conversely, NO2 levels were lower in umbilical artery blood. Umbilical vein endothelial cells (HUVEC) from the same pregnancies presented a less active endothelial nitric oxide synthase (eNOS) with a lower release of NO2. Increased NO2 and decreased NOHb umbilical levels coincided with intra-partum hypoxia. Hypoxic newborns manifested a post-natal reduction of NOHb with a greater yield of NO2. Pregnancies concluded with labour present an activation of the NO system with a functional modification of both feto-placental endothelial cells and the fetus. Post-natal NO2 levels are changed concomitantly. This set of responses may reflect an adaptive process to preserve the vaginally born babies from respiratory problem. The intrapartum oxidative stress may be associated with a specific protective influence on brain energy metabolism under conditions where a critical O2 deficiency is present.