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阻断大鼠基底动脉和两侧颈总动脉造成全脑缺血前１５ｍｉｎ给大鼠腹腔注射氯胺酮（５ｍｇ／１００ｇ），以探讨氯胺酮对大鼠全脑缺血／再灌注损伤的影响与机理。结果表明，与再灌组比较，氯胺酮组的脑含水量和Ｎａ＋含量显著降低（Ｐ＜０．０１，Ｐ＜０．０１），Ｋ＋含量有所增加，但差别无显著性（Ｐ＞０．０５），乳酸脱氢酶和磷酸肌酸激酶活性显著升高（Ｐ＜０．０１，Ｐ＜０．０１），乳酸积聚显著减少（Ｐ＜０．０１），丙二醛含量显著降低（Ｐ＜０．０ｌ），脑电波抑制未见恢复．提示氯胺酮对大鼠全脑缺血／再灌注损伤有明显保护作用，因而认为兴奋性氨基酸参与脑缺血／再灌注损伤的发生机理．
The rats were injected intraperitoneally with ketamine (5mg / 100g) 15min before occlusion of the basilar and bilateral common carotid arteries in order to investigate the effect and mechanism of ketamine on global cerebral ischemia / reperfusion injury in rats. The results showed that compared with reperfusion group, brain water content and Na + content in ketamine group were significantly decreased (P <0.01, P <0.01), K + content increased, but the difference was not significant (P> 0. (P <0.01, P <0.01), lactate accumulation decreased significantly (P <0.01), MDA content decreased significantly (P <0.01, P < <0.0l), no suppression of brainwave suppression. It is suggested that ketamine has a significant protective effect on global cerebral ischemia / reperfusion injury in rats. Therefore, excitatory amino acids are involved in the pathogenesis of cerebral ischemia / reperfusion injury.