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目的：观察异丙嗪（ｐｒｏｍｅｔｈａｚｉｎｅ，ＰＭＺ）对家兔ＥＧＴＡ性发热的影响并探讨其作用机制。方法：侧脑室和静脉给药。用Ｆｕｒａ－２荧光分光光度法测定细胞内游离钙浓度（［Ｃａ２＋］ｉ）。结果：（１）侧脑室灌注０６μｍｏｌＥＧＴＡ引起家兔明显的发热反应，侧脑室灌注０６μｍｏｌＥＧＴＡ２０ｍｉｎ后，静脉注射ＰＭＺ（５ｍｇ／ｋｇ）明显抑制ＥＧＴＡ引起的结肠温度上升，其３ｈ发热反应指数明显低于侧脑室灌注０６μｍｏｌＥＧＴＡ２０ｍｉｎ后静脉注射生理盐水（ＮＳ）组。而侧脑室灌注人工脑脊液（ＡＣＳＦ）２０ｍｉｎ后静脉注射ＰＭＺ（５ｍｇ／ｋｇ）组家兔结肠温度明显低于ＡＣＳＦ＋ＮＳ对照组。（２）体外实验发现，向下丘脑细胞悬液中加入终浓度为０７４ｍｍｏｌ／Ｌ的ＰＭＺ，下丘脑细胞［Ｃａ２＋］ｉ从（１５９２±１８８）ｎｍｏｌ／Ｌ升高到（５３３７±９０１）ｎｍｏｌ／Ｌ（Ｐ＜００５）。结论：ＰＭＺ诱导体温调节中枢神经细胞［Ｃａ２＋］ｉ升高可能是ＰＭＺ抑制家兔ＥＧＴＡ性发热的中枢机制之一。
Objective: To observe the effect of promethazine (PMZ) on EGTA fever in rabbits and to explore its mechanism. Methods: Intracerebroventricular and intravenous administration. Intracellular free calcium concentration ([Ca 2+] i) was determined by Fura-2 fluorescence spectrophotometry. Results: (1) Intracerebroventricular perfusion with 0.6 μmol EGTA caused a significant fever response in rabbits. Intraventricular perfusion with 0.6 μmol EGTA for 20 min, intravenous injection of PMZ (5 mg / kg) significantly inhibited the colonic temperature induced by EGTA, Lower than the lateral ventricle perfusion 0 6μmolEGTA20min after intravenous injection of saline (NS) group. However, the colonic temperature of rabbits injected with PMZ (5mg / kg) intravenously 20 minutes after intracerebroventricular injection of artificial cerebrospinal fluid (ACSF) was significantly lower than that of ACSF + NS control group. (2) In vitro, it was found that PMZ was added to the hypothalamus cell suspension at a final concentration of 074 mmol / L, and the [Ca2 +] i of hypothalamic cells increased from (1592 ± 188) nmol / L to 533 7 ± 90 1) nmol / L (P <0 05). CONCLUSION: PMZ-induced thermoregulation of [Ca2 +] i in central nervous system may be one of the central mechanisms by which PMZ inhibits EGTA-induced fever in rabbits.