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本文用脑室灌注和Ｆｕｒａ２测定细胞内游离钙技术观察了地塞米松（ｄｅｘａｍｅｔｈａｓｏｎｅ，ＤＥＸ）对家兔乙二醇双（２氨基乙醚）四乙酸性发热效应和下丘脑细胞内游离钙浓度（［Ｃａ２＋］ｉ）的影响，借此深入探讨地塞米松解热作用的中枢机制。结果发现：脑室灌注乙二醇双（２氨基乙醚）四乙酸（０６ｎｍｏｌ）引起家兔结肠温度明显升高，静脉注射地塞米松（５ｍｇ／ｋｇ）显著抑制家兔乙二醇双（２氨基乙醚）四乙酸性发热，地塞米松（６０～１２０μｍｏｌ／Ｌ）并不影响下丘脑细胞内［Ｃａ２＋］ｉ，而事先脑室灌注抑制基因转录的放线菌素Ｄ（３ｎｍｏｌ）则完全取消了地塞米松对乙二醇双（２氨基乙醚）四乙酸性发热的解热作用。这些结果提示：地塞米松显著抑制家兔乙二醇双（２氨基乙醚）四乙酸性发热，其机制与地塞米松激活脑内某些基因的表达有关，而与下丘脑神经细胞跨膜钙离子流无关。
In this paper, intracellular perfusion and Fura 2 intracellular free calcium determination of dexamethasone (dexamethasone, DEX) in rabbits ethylene glycol bis (2-aminoethyl ether) tetraacetic acid fever and hypothalamic intracellular free calcium concentration ([Ca2 +] i), to explore in depth the central mechanism of dexamethasone’s antipyretic effect. The results showed that intravenous injection of dexamethasone (5 mg / kg) significantly inhibited the growth of rabbits with ethylene glycol bis (2-aminoethyl ether) tetraacetic acid (0.6 nmol) 2-aminoethyl ether) tetraacetic acid fever, dexamethasone (60 ~ 120μmol / L) does not affect the intracellular [Ca2 +] i in the hypothalamus, while preinventricular perfusion inhibition of actinomycin D (3nmol) Dexamethasone abolished the antipyretic effect of ethylene glycol bis (2-aminoethyl ether) tetraacetic acid fever. These results suggest that dexamethasone significantly inhibits ethylene glycol bis (2-aminoethyl ether) tetraacetic acid-induced fever in rabbits. The mechanism of dexamethasone is related to the activation of some genes in dexamethasone-activated brain, but not to the hypothalamic neuronal transmembrane Calcium ion flow has nothing to do.