Spinal potentiation and supraspinal additivity in the antinociceptive interaction between systemically administered alpha 2-adrenoceptor agonist and cocaine in the rat.
Spinal potentiation and supraspinal additivity in the antinociceptive interaction between systemically administered alpha 2-adrenoceptor agonist and cocaine in the rat.
复制标题
大鼠全身给予α2-肾上腺素受体激动剂和可卡因之间的抗伤害相互作用中的脊髓增强和脊髓上加性。
DOI：
10.1213/00000539-199408000-00010
复制
发表时间：
1994
影响因子：
5.7
通讯作者：
M. M. Hämäläinen
中科院分区：
文献类型：
--
作者：
A. Pertovaara;M. M. Hämäläinen
我们在大鼠甩尾和热板试验中研究了全身给予美托咪定（一种选择性α 2-肾上腺素受体激动剂）与可卡因的抗伤害性相互作用。在完整大鼠中，美托咪定单药（25-300 μ g/kg皮下注射[SC]）和可卡因单药（10-30 mg/kg腹腔注射[IP]）在棘上介导的热板试验中产生剂量依赖性抗伤害感受，其联合（美托咪定25 μ g/kg+可卡因10-20 mg/kg）产生累加抗伤害感受作用。在脊髓介导的甩尾试验中，仅美托咪定单独给药在完整大鼠和脊髓大鼠中均产生显著的抗伤害感受作用，而可卡因单独给药仅在最高剂量（30 mg/kg）下且仅在完整大鼠中在甩尾试验中产生轻微显著的抗伤害感受作用。美托咪定（25 μ g/kg SC）与可卡因（10-20 mg/kg IP）联合给药在完整大鼠和脊髓大鼠的甩尾试验中均产生了抗伤害感受增强作用。结果表明，在脊髓上的水平有一个添加剂之间的抗伤害性相互作用可卡因和美托咪定，而在脊髓水平可卡因增强美托咪定诱导的抗伤害性独立的脊髓上的机制。这些结果进一步支持了以前的证据，表明单独全身给药的α 2-肾上腺素能药物产生的抗伤害作用主要是由于脊髓机制，而单独全身给药的可卡因主要是由于脊髓上机制。
We studied the antinociceptive interaction of systemically administered medetomidine, a selective alpha 2-adrenoceptor agonist, with cocaine in the tailflick and hotplate tests in rats. In intact rats, both medetomidine alone (25-300 micrograms/kg subcutaneously [SC]) and cocaine alone (10-30 mg/kg intraperitoneally [IP]) produced a dose-dependent antinociception in the supraspinally mediated hotplate test, and their combination (medetomidine 25 micrograms/kg+cocaine 10-20 mg/kg) produced an additive antinociceptive effect. In the spinally mediated tailflick test, only medetomidine alone produced a significant antinociceptive effect both in intact and spinal rats, whereas cocaine alone produced a marginally significant antinociceptive effect in the tailflick test only at the highest dose used (30 mg/kg) and only in intact rats. The combination of medetomidine (25 micrograms/kg SC) with cocaine (10-20 mg/kg IP) produced potentiation of antinociception in the tailflick test both in intact and spinal rats. The results indicate that at the supraspinal level there is an additive antinociceptive interaction between cocaine and medetomidine, whereas at the spinal level cocaine potentiates the medetomidine-induced antinociception independent of supraspinal mechanisms. The results further support previous evidence indicating that antinociception produced by a systemically administered alpha 2-adrenergic drug alone is mainly due to spinal mechanisms, whereas that by systemically administered cocaine alone is mainly due to supraspinal mechanisms.