Mousa S, Miller C H, Couri D
Psychopharmacology (Berl). 1983;79(2-3):199-202. doi: 10.1007/BF00427812.
Analgesia induced in rats by cold-water swim stress and measured by the tail-flick and hot-plate methods was significantly antagonized after IP pretreatment for 3 days with 8 mg/kg dexamethasone. The analgesia developed by the cold-water swim stressor was also attenuated by 1 mg/kg naloxone. These results suggest that the corticosteroids may have a role in modulating stress-induced analgesia and that the adrenal-pituitary axis modulates the endogenous opiate system. These conclusions are based on recent reports that indicate the release of the opiate-like peptide beta-endorphin and adrenocorticotropin (ACTH) from the pituitary are increased by acute stress and inhibited by administration of the synthetic glucocorticoid dexamethasone.
通过冷水游泳应激在大鼠中诱导产生的、并通过甩尾和热板法测量的镇痛作用,在用8毫克/千克地塞米松腹腔注射预处理3天后受到显著拮抗。1毫克/千克纳洛酮也减弱了冷水游泳应激源产生的镇痛作用。这些结果表明,皮质类固醇可能在调节应激诱导的镇痛中起作用,并且肾上腺-垂体轴调节内源性阿片系统。这些结论基于最近的报告,这些报告表明,急性应激会增加垂体中阿片样肽β-内啡肽和促肾上腺皮质激素(ACTH)的释放,而合成糖皮质激素地塞米松的给药会抑制这种释放。