Role of Nitric Oxide in the Regulation of the Cerebral Circulation in the Lamb Fetus during Normoxemia and Hypoxemia

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Abstract
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 Nω-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/100g/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/l00 g/min, p < 0.05). This vasodilatory response was largely blocked after NNLA (Q 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.

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