The role of nitric oxide synthesis in cardiovascular responses to acute hypoxia in the late gestation sheep fetus.

1. In fetal sheep (123-129 days gestation) we investigated the effect of acute isocapnic hypoxia (Pa,O2, 12 +/- 0.6 mmHg) on the fetal heart rate (FHR), mean systemic arterial blood pressure (MAP), carotid blood flow (CBF), femoral blood flow (FBF), carotid vascular resistance (CVR) and femoral vascular resistance (FVR) with the infusion of either the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or saline vehicle. 2. During normoxia, CBF was lower (P < 0.05) and MAP, FVR and CVR were higher with L-NAME than with vehicle infusion (P < 0.01, P < 0.05 and P < 0.01, respectively). FHR fell 15 min after the onset of L-NAME infusion (P < 0.05). During hypoxia in both groups, FHR showed an initial rapid fall (P < 0.05) and subsequent return to prehypoxic levels, and there was a fall in FBF (P < 0.01). MAP increased during hypoxia with vehicle (P < 0.05) but not L-NAME infusion: thus MAP was similar during hypoxia in the two groups. The rebound tachycardia seen during recovery in the vehicle group (P < 0.01) was not evident in the L-NAME group. The rise in CBF and fall in CVR during hypoxia with vehicle (P < 0.01 and P < 0.05, respectively) was absent with L-NAME infusion. FVR rose during hypoxia in both groups (P < 0.05). 3. Thus NOS inhibition alters basal systemic vascular tone in the late gestation fetus. The rise in CBF and fall in CVR during hypoxia is absent with NOS inhibition.