| Objective:To explore the neuroprotective effects of phenytoin sodium and its possible mechanisms in patients with acute cerebral infarction.Methods:60 patients were randomly divided into control group and group treated with Phenytoin sodium. In all patients clinical neurological deficits were assessed; the level of serum S-100βprotein was determined through ELISA; the level of serum NO was determined through nitrate reductase method; the level of serum MDA and SOD were determined through colorimetric method before and after treatment. And half of them were observed the effect on rCBF by SPECT brain perfusion imaging. Semiquantitative analysis of rCBF was processed with normal/focus mirror regions ratio on transverse images.Results:The scores of clinical neurological deficits were respectively 20.6±5.6 and 10.7±6.8 before and after treatment in group treated with Phenytoin sodium. The scores were respectively 21.5±5.1 and 14.6±6.7 in control group. The clinical therapeutic effect of Phenytoin was better than control group(P<0.05). The levels of serum S-100βwere respectively 0.69±0.24μg/ L and 0.31±0.16μg/ L before and after treatment in group treated with Phenytoin sodium. S-100βwere respectively 0.67±0.27μg/ L and 0.41±0.20μg/ L in control group. The level of serum S-100βwas significantly lower(P<0.05), compared with control group after treatment. The levels of serum NO were respectively 93.6±14.0μmol/L and 72.0±10.7μmol/L before and after treatment in group treated with Phenytoin sodium. NO were respectively 97.1±13.7μmol/L and 78.2±11.2μmol/L in control group. The level of serum NO was significantly lower(P<0.05), compared with control group after treatment. The levels of serum MDA were respectively 7.5±2.1nmol/ml and 5.1±1.9nmol/ml before and after treatment in group treated with Phenytoin sodium. MDA were respectively 7.6±2.3nmol/ml and 6.1±2.0nmol/ml in control group. The level of serum MDA was significantly lower(P<0.05), compared with control group after treatment. The levels of serum SOD were respectively 80.5±19.2U/ml and 102.1±19.0U/ml before and after treatment in group treated with Phenytoin sodium. SOD were respectively 78.7±18.0U/ml and 91.3±17.2U/ml in control group. The level of serum SOD was significantly higher(P<0.05), compared with control group after treatment. Semiquantitative values of rCBF(R) were respectively 1.231±0.068 and 1.113±0.057 before and after treatment in group treated with Phenytoin sodium. R were respectively 1.226±0.074 and 1.159±0.054 in control group. Regional cerebral blood flow was significantly improved(P<0.05), compared with control group after treatment.Conclusion:Phenytoin sodium has neuroprotective effect on cerebral ischemic injury .Phenytoin sodium can improve clinical neurological deficits; decrease levels of serum S-100β,NO,MDA and increase serum SOD activity in patients with acute cerebral infarction. Phenytoin sodium may protect brain tissues from cerebral ischemic injury by inhibiting formation of free radical, anti-lipid peroxidation and improving regional cerebral blood flow.Phenytoin sodium may be a possible,safe and valid neuroprotective strategy in patients with acute cerebral infarction. |
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