Establishment of the estimation method for analgesia using stress-induced hyperalgesic animals

1.坎布族药物毛乌素口服液100 mg/kg和300 mg/kg对反复冷应激(RCS)引起的大鼠和小鼠痛觉过敏有抗伤害作用，而对健康小鼠无明显作用。吗啡(0.1-3 mg/kg，S.C.)和双氯芬酸(0.5-80 mg/kg，P.O.)鞘内注射5，7-二羟色胺(5，7-DHT)可显著抑制RCS大鼠的抗伤害性感觉，但不能被肾上腺素能神经毒素6-OHDA(6-OHDA)阻断。3.鞘内注射5，7-二羟色胺、5，7-二羟色胺(5，7-DHT)能拮抗儿茶酚胺能神经毒素(6-OHDA)可显著抑制RCS大鼠的抗伤害性感觉。3.鞘内注射5-羟色胺、5-羟色胺、甲硫氨酸和甲基丝氨酸受体拮抗剂，可显著抑制RCS大鼠的抗伤害性感觉。6.鞘内注射6-OHDA可抑制痛觉过敏大鼠的痛觉感受，而5，7-二羟色胺(5，7-DHT)对痛觉过敏大鼠的镇痛作用不明显。此外，这些发现还表明，毛刺-布施-赛辛托和凯时-托的抗伤害性作用可能至少部分分别由下行的5-羟色胺能系统和下行的去甲肾上腺素能系统介导。

1, The Kampo medicine Maoh-Bushi-Saishin -toh at peroral doses of 100 and 300 mg/kg produced an antinociception in rats and mice that showed hyperalgesia induced induced by repeated cold stress (RCS), without effect in healthy ones. Morphine (0.1-3 mg/kg, s.c.) and diclofenac (0.5-80 mg/kg, p.o.) also produced an antinociception in RCS animals.2, The antinociception of Maoh-Bushi-Saishin-toh (300 mg-kg, ) in the RCS rat was significantly suppressed by intrathecal pretreatment with the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) but not with the catecholaminergic neurotoxin, 6-hydroxydopamine (6-OHDA).3, The antiociception of Maoh-Bushi-Saishin-toh (300 mg/kg) in the RCS rat was significantly suppressed by intrathecal injection with antagonists for serotonin receptors, cyproheptadine, methiotepine and methysergide, but not with an antagonist for adrenaline receptors, phentolamine.4, The Kampo medicine Keishi-toh at peroral doses of 100 and 300 mg-kg produced an antinociception in rats that showed hyperalgesia induced by RCS,without effect in healthy ones.5, The intrathecal pretreatment with 6-OHDA tended to suppress the antinociception of Keishi-toh (300 mg/kg) in the RCS rat, but 5,7-DHT had no effect on the antinociception of Keishi-toh.6, As mentioned above, we detected antinociceptive effects of Maoh-Bushi-Saishin-toh and Keishi-toh using RCS-induced hyperalgesic animals. In addition, these findings suggest that the antinociception of Maoh-Bushi-Saishin-toh and Keishi-toh may be at least in part mediated by the descending serotonergic and the descending noradrenergic systems, respectively.