Cai B, Huang X, Wang G, Mo W
Department of Neurobiology, Shanghai Medical University.
Zhen Ci Yan Jiu. 1994;19(1):66-70, 74.
The present study was to investigate the effect of metoclopramide (MCP) on electroacupuncture analgesia (EAA) and its mechanism on a rabbit visceral pain model. The results showed that MCP 8mg/kg i.v. could potentiate EAA and prolong the analgesic duration. The potentiation effect could be attenuated by icv apomorphine (APO) (a mixed D1/D2 agonist). The analgesic duration was shortened by icv SKF38393 (a selective D1 agonist) or LY171555 (a selective D2 agonist). Using HPLC-ECD, we also found that the HVA content in CSF significantly increased at 20 min. after electroacupuncture (EA) or MCP 8mg/kg i.v. (P < 0.05), but the change of HVA content was not significant when EA and MCP 8mg/kg i.v. were used together. All these observations indicate that MCP have effects of potentiating EAA and prolonging analgesic duration. These effects are related to the blockade of the central DA receptor. The activations of D1 or D2 receptor is unfavourable to the expression of EA after effect.
本研究旨在探讨甲氧氯普胺(MCP)对兔内脏痛模型电针镇痛(EAA)的影响及其机制。结果表明,静脉注射8mg/kg MCP可增强EAA并延长镇痛持续时间。脑室注射阿扑吗啡(APO,一种D1/D2混合激动剂)可减弱这种增强作用。脑室注射SKF38393(一种选择性D1激动剂)或LY171555(一种选择性D2激动剂)可缩短镇痛持续时间。使用高效液相色谱-电化学检测法(HPLC-ECD),我们还发现电针(EA)或静脉注射8mg/kg MCP后20分钟,脑脊液中高香草酸(HVA)含量显著增加(P<0.05),但EA与静脉注射8mg/kg MCP联合使用时,HVA含量变化不显著。所有这些观察结果表明,MCP具有增强EAA和延长镇痛持续时间的作用。这些作用与中枢多巴胺(DA)受体的阻断有关。D1或D2受体的激活不利于电针后效应的表达。