摘要
以创伤性脑水肿的大鼠模型对作者提出的药理剂量的糖皮质激素（ＧＣ）通过低亲和力糖皮质激素受体（ＧＲＬ）的介导发挥治疗作用的假说作了验证。结果发现，只有当血浆地塞米松（Ｄｃｘ）浓度达到１０（－６）ｍｏｌ／Ｌ（与ＧＲＬ的Ｋｄ同一数量级）时才能使脑水肿减轻，这减轻作用可被糖皮质激素受体的竞争性拮抗剂ＲＵ４８６所逆转，符合于我们的假说。
We ha ve proposed that the therapeutic effects of the massive dose ofglucoco rticoid (GC)might be mediated by low affinity glucocortico id reeeptor(GRL),pre-sent work was undertaken tO testify this hypothesis in rats with traumatic edema.Traumaticedema was alleviated significantly in rats y i.v,injection of massive dose ofdexamethasone(Dex)(5.0mg/kg b.w),but not 0.5mg/kg bw,The alleviation can be reversedcompletely by RU486,a competitive antagonist of high-and low-afflnity GR. Theconcentrations of Dex in plasma were in the order of 10(-6) and 10(-7)mol/L after injection of massive and small dose of Dex respectively.Sinee the Kd of the high-and low affinityGW is in the order of 10(-8) and 10(-6) mol/L respectively,it might be predicted that thetherapeutic effect of the massive dose of GC should be mediated by GRL,and that thesmall dose of Dex is not effective because of the decrease of the high affinity GR aftertrauma which was reported by us previously.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1996年第4期384-386,共3页
Chinese Journal of Pathophysiology
关键词
脑水肿
糖皮质激素
地塞米松
Brain edema·Receptor,glucocorticoid·Dexamethasone·Rats
