Attenuation of brain edema, blood-brain barrier breakdown, and injury volume by ifenprodil, a polyamine-site N-methyl-D-aspartate receptor antagonist, after experimental traumatic brain injury in rats.

摘要: OBJECTIVE Traumatic brain injury (TBI) has been shown to induce a significant change in polyamine metabolism. Polyamines and polyamine-dependent calcium influx play an important role mediating the effects of excitotoxic amino acids at N-methyl-D-aspartate (NMDA) receptor site. We studied ifenprodil, known as noncompetitive inhibitor sites NMDA receptor, on edema formation, blood-brain barrier breakdown, volume after TBI. METHODS Experimental TBI was induced Sprague-Dawley rats by controlled cortical impact device, functioning velocity 3 m/s produce 2-mm deformation. Ifenprodil or saline (10 mg/kg) injected intraperitoneally immediately then every 90 minutes until 6 hours Blood-brain breakdown evaluated quantitatively fluorometric assay Evans blue extravasation. Brain water content, indicator edema, measured with wet-dry method 24 Injury quantitated from slices stained 2% cresyl violet solution 7 days RESULTS significantly lower traumatic cortex ifenprodil-treated group than saline-treated (84.4 +/- 26.8 microg/g versus 161.8 27 microg/g, respectively, P < 0.05). reduced relative that (80.9 0.5% 82.4 0.6% treatment (14.9 8.1 mm3 24.4 6.7 mm3, CONCLUSION The polyamine-site antagonist ifenprodil affords neuroprotection model may hold promise for discovery mechanism delayed neurological deficits