可乐定镇痛与中枢Ca2+的关系

用大鼠甩尾法和放射配基结合实验,探讨了可乐定镇痛与中枢Ca²⁺的关系。CaCl₂(1μmol/rat,icv)和EGTA(0.2μmol/rat,icv)分别拮抗和增强可乐定(1mg/kg,sc)的镇痛。戊脉安(0.1μmol/rat,icy)对可乐定(1 mg/kg,sc)镇痛无明显影响,但可部分翻转CaCl₂对可乐定镇痛的拮抗。CaCl₂(1×10^-3mol)对[³H]-可乐定结合无明显抑制。结果表明可乐定镇痛与脑室周围组织中Ca²⁺浓度变化密切相关,Ca²⁺至少部分需经对戊脉安敏感的钙通道进入细胞内方可拮抗可乐定镇痛。推沦:可乐定镇痛与神经元内Ca²⁺有关。

RELATIONSHIP BETWEEN CLONIDINE ANALGESIA AND CALCIUM CATION

Using radiant heat tail flick method and radioactive ligand binding test, the relationship between clonidine analgesia and central calcium cation was studied in rats. The analgesia of clonidine (1 mg/kg, sc) was antagonized by CaCl₂(1μmol/rat, icv) and potentiated by EGTA (0.2 μmol/rat, icv), a calcium chelator. Though the pretreatment with verapamil (0.1 μmol/rat, icv) showed no significant influence on the analgesia of clonidine (1 mg/kg, sc), it partly reversed the antagonistic effect of calcium. Calcium exhibited no inhibiting effect on [³H]-clonidine binding at the concentrations 1 × 10^-7～1 × 10^-3 mol/L. The results suggest that analgesia of clonidine is closely rrelated with the calcium level of the tissue around the ventricles of brain. We consider that clonidine analgesia involves in central calcium, we also postulate that calcium takes part in a physiologic—biochemical process which is shared by the activated receptors in the endogenous analgesia system.