L-arginine partially restores the diminished CO2 reactivity after mild controlled cortical impact injury in the adult rat.

Using an open cranial window technique, the authors investigated the mechanisms associated with the suppressed CO2 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.