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 (Qbrain-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 (Rcer) 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 (Qbrain-tot from 129 +/- 25 to 89 +/- 26 ml/100 g/min, p < 0.05; Rcer from 0.46 +/- 0.03 to 0.80 +/- 0.09 mm Hg/ml/100 g/min, p < 0.05). During hypoxemia before NNLA infusion, Qbrain-tot increased (from 129 +/- 25 to 187 +/- 56 ml/100 g/min, p < 0.05), and Rcer 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 (Qbrain-tot 143 +/- 45 ml/100 g/min; Rcer 0.58 +/- 0.07 mm Hg/ml/100 g/min). The response to hypoxemia was restored after infusion of L-arginine (Qbrain-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.