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Using an open cranial window technique, the authors investigated the mechanisms associated with the suppressed CO 2  reactivity after mild controlled cortical impact (CCI) injury in rats. The dilation of arterioles (n = 7) to hypercapnia before injury was 38 ± 12%, which was significantly reduced both at 1 hour (23 ± 15% dilation) and at 2 hours after injury (11 ± 19% dilation). In the presence of L-arginine (10 mmol/L topical suffusion, 300 mg/kg intravenous infusion), the dilation of pial arterioles (n = 6) to hypercapnia was partially restored to 30 ± 6% at 2 hours after injury. In the presence of the nitric oxide (NO) donor, S-nitroso- N-acetylpenicillamine (SNAP) (10 −8  mol/L topical suffusion), the dilation of pial arterioles (n = 5) to hypercapnia remained diminished (5 ± 7%) at 2 hours after injury. The dilation of pial arterioles (n = 4) to hypercapnia also remained suppressed (5 ± 6%) with topical suffusion of the free radical scavengers, polyethylene glycol-superoxide dismutase (60 units/mL) and polyethylene glycol-catalase (40 units/mL). The authors have shown that L-arginine at least partially restores the diminished response to hypercapnia after mild CCI injury. Furthermore, these data suggest that the beneficial effects of L-arginine are mediated by a combination of providing substrate for NO synthase and scavenging free radicals.

L-Arginine Partially Restores the Diminished CO2 Reactivity after Mild Controlled Cortical Impact Injury in the Adult Rat

L-Arginine Partially Restores the Diminished CO₂ Reactivity after Mild Controlled Cortical Impact Injury in the Adult Rat