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We investigated the changes in nitric oxide (NO) concentration in the brain of the rabbit by measuring NO-related electrical current. Seventeen Japanese white rabbits were anesthetized with pentobarbital sodium and mechanically ventilated with tracheotomy tubes. An NO-selective electrode was used for the detection of NO. After a round craniotomy in the left parietal lobe, an NO-sensitive electrode was placed in the brain. Rabbits were hemorrhaged to a mean arterial blood pressure of 35 ± 7 mmHg, from a baseline of 112 ± 12 mmHg (mean ± SD). The shock was maintained for 5 min. The mean extracted blood volume was 77 ± 17 mL. Then, retransfusion of shed blood caused a rapid restoration of mean arterial blood pressure. The amount of time required to induce hemorrhagic shock was 261 ± 34 s. The time required to retransfuse the extracted blood was 233 ± 43 s (p > .05). During shock, the NO-selective electrode produced an extensive increase in current, from 110 ± 94.5 pA to 1010 ± 543 pA (mean ± SD, p < .001). The current continued to increase for a few minutes after the recovery from shock, with a maximal increase reaching 1245 ± 515 pA (p < .001). This enhanced release of NO-related current (1,132%) recovered to the baseline level at 44 ± 7 min after retransfusion. When the same investigation was performed on the same animals on which had been placed the same electrode pretreated with NG-nitro-L-arginine methylester (L-NAME) 30 mg/kg intravenously, NO-related current increased from 101 ± 158 to a maximum of 860 ± 406 pA (752%). Our results suggest that NO may play an important role in the brain during the early period of hemorrhagic shock, and that L-NAME 30 mg/kg intravenously might not inhibit the NO production in the parietal lobe, probably due to a blood-brain barrier to the nitric oxide synthase-inhibiting drug.