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 reg ional cerebral blood flow (rCBF) during hypoxia and reoxygenation in d eveloping rat striatum. The subjects were urethane-anesthetized 7- and 14-d-old rats. After 120 min of baseline measurements, the rats recei ved an i.p. injection of either saline (as a control) or an NO synthas e 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% O- 2, followed by a 60-min recovery in 21% O-2, rCBF and NO concentration in the striatum were measured by laser Doppler flowmetry and an NO el ectrode throughout the experimental period. In the controls, rCBF decr eased 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-NA ME attenuated the hyperemic response to hypoxia/reoxygenation in both ages (n = 11, in each age). Striatal NO production increased during hy poxia and reoxygenation in both ages, but the increase was significant ly less in 7-d-old than in 14-d-old rats. The NO increase was associat ed with the increase in rCBF, and both were attenuated by L-NAME. We s peculate that NO release during hypoxia/reoxygenation modulates rCBF. The immature young rat brain may have less capacity to activate NO pro duction than the more developed brain.