ROLE OF NITRIC-OXIDE IN THE REGULATION OF THE CEREBRAL-CIRCULATION IN THE LAMB FETUS DURING NORMOXEMIA AND HYPOXEMIA

The influence of nitric oxide (NO) blockade on resting tone and on hypoxia-induced vasodilatation of the cerebral vascular bed was examined in chronically instrumented lamb fetuses. Total (Q(brain-tot)) and regional brain blood flow were measured using radioactive microspheres. NO blockade was achieved by N-omega-nitro-L-arginine (NNLA) infusion into the carotid artery via a lingual artery. Fetal cerebral blood flow and cerebral vascular resistance (R(cer)) were determined during normoxemia and hypoxemia and before and during infusion of L-arginine. During normoxemia, the brain blood flow decreased, and the resistance increased significantly after NNLA infusion (Q(brain-tot) from 129 +/- 25 to 89 +/- 26 ml/100 g/min, p < 0.05; R(cer) from 0.46 +/- 0.03 to 0.80 +/- 0.09 mm Hg/ml/100 g/min, p < 0.05). During hypoxemia before NNLA infusion, Q(brain-tot) increased (from 129 +/- 25 to 187 +/- 56 ml/ 100 g/min, p < 0.05), and R(cer) decreased (from 0.46 +/- 0.03 to 0.39 +/- 0.07 mm Hg/ml/100 g/min, p < 0.05). This vasodilatory response was largely blocked after NNLA(Q(brain-tot) 143 +/- 45 ml/100 g/min; R(cer) 0.58 +/- 0.07 mm Hg/ml/100 g/min). The response to hypoxemia was restored after infusion oft arginine (Q(brain-tot) 180 +/- 47 ml/100 g/min). The resting tone of the cerebral vascular bed of the lamb fetus is under NO control, and NO mediates the cerebral vasodilatory response to hypoxia in the lamb fetus.