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为检测头部重点低温脱水综合疗法（ＳＨＣＤＣＴ）能否消除激动性氨基酸神经毒性，观察了完 全性脑缺血（四血管式，３０分钟）后再灌注 ３０、１８０和 ３６０分钟（ｎ＝８）时颞叶组织中谷氨酸（Ｇｌｕ）、门冬氨 酸（Ａｓｐ）含水量和葡萄糖等的变化，比较了头部重点低温（ＳＨＣ，２８℃，体表降温法）、甘露醇脱水和 ＳＨＣＤＣＴ三种治疗对这些变化的影响。发现与未缺血动物相比，再灌注后Ａｓｐ、Ｇｌｕ和含水量升高（Ｐ＜ ０．０１ ），葡萄糖减少（Ｐ＜０． ０１），ＳＨＣ和 ＳＨＣＤＣＴ显著抑制这些变化（Ｐ＜０． ０１），促进它们尽快恢复到未 缺血水平。结果提示：再灌注后尽早实施ＳＨＣＤＣＴ仍能有效缓解激动性氨基酸神经毒性，这可能是 ＳＨＣＤＣＴ脑复苏机制之一。
To examine whether head-key hypothermic dehydration combined therapy (SHCDCT) abolishes agonistic amino acid neurotoxicity, reperfusion was observed at 30, 180 and 360 minutes (n = 8) following complete cerebral ischemia (IVA, 30 minutes) The contents of glutamic acid (Glu), aspartic acid (Asp) and glucose in the temporal lobe tissue were compared. The results of SHC (28 ℃, body surface temperature reduction), dehydration of mannitol and SHCDCT The impact of treatment on these changes. Compared with non-ischemic animals, the changes of Asp, Glu and water content (P <0.01) and glucose decreased (P <0.01) after reperfusion, SHC and SHCDCT significantly inhibited these changes (P < 01), to promote them as soon as possible to return to the level of ischemia. The results suggest that SHCDCT after reperfusion can effectively relieve the neurotoxicity of agonistic amino acids, which may be one of the mechanisms of SHCDCT brain resuscitation.