Effects of hypoxia and reoxygenation on nitric oxide production and cerebral blood flow in developing rat striatum.

We investigated the role of nitric oxide (NO) in the regulation of regional cerebral blood flow (rCBF) during hypoxia and reoxygenation in developing rat striatum. The subjects were urethane-anesthetized 7- and 14-d-old rats. After 120 min of baseline measurements, the rats received an i.p. injection of either saline (as a control) or an NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) 30 min before hypoxia. Then they were subjected to a 60-min hypoxia in 8% O2, followed by a 60-min recovery in 21% O2. rCBF and NO concentration in the striatum were measured by laser Doppler flowmetry and an NO electrode throughout the experimental period. In the controls, rCBF decreased to 93 +/- 3% of baseline during hypoxia and increased to 124 +/- 3% of baseline during reoxygenation in 7-d-old rats (n = 13), whereas rCBF increased during both hypoxia and reoxygenation in 14-d-old rats to 125 +/- 6% and 168 +/- 6% of baseline, respectively (n = 17). L-NAME attenuated the hyperemic response to hypoxia/reoxygenation in both ages (n = 11, in each age). Striatal NO production increased during hypoxia and reoxygenation in both ages, but the increase was significantly less in 7-d-old than in 14-d-old rats. The NO increase was associated with the increase in rCBF, and both were attenuated by L-NAME. We speculate that NO release during hypoxia/reoxygenation modulates rCBF. The immature young rat brain may have less capacity to activate NO production than the more developed brain.