一氧化氮合酶的抑制增强了吗啡在大鼠脊髓中的镇痛作用。
Inhibition of nitric oxide synthase enhances morphine antinociception in the rat spinal cord.
作者信息
Przewłocki R, Machelska H, Przewłocka B
机构信息
Neuropeptide Research Department, Polish Academy of Sciences, Kraków.
出版信息
Life Sci. 1993;53(1):PL1-5. doi: 10.1016/0024-3205(93)90615-a.
NG-nitro-L-arginine methyl ester (L-NAME, 400-1500 micrograms), administered intrathecally (ith.), elicits a slight but dose-related antinociception in rats, assessed by tail-flick and paw pressure tests. L-NAME (400 micrograms) and morphine (0.5 microgram) coadministered ith. elicit a profound and long-lasting antinociception, which is abolished by ith. administration of 3-morpholino-sydnonimine (SIN-1, 100 micrograms). Hemoglobin (266 micrograms) administered ith. also slightly potentiates morphine antinociception. These results suggest that nitric oxide (NO) is involved in spinal nociceptive events, and that the increased production of NO following the nociceptive input may diminish the efficiency of opioid antinociception in the spinal cord.
鞘内注射N-硝基-L-精氨酸甲酯（L-NAME，400 - 1500微克）可在大鼠中引发轻微但与剂量相关的抗伤害感受，通过甩尾和爪压试验进行评估。鞘内共同注射L-NAME（400微克）和吗啡（0.5微克）可引发深刻且持久的抗伤害感受，而鞘内注射3-吗啉代西多明（SIN-1，100微克）可消除这种感受。鞘内注射血红蛋白（266微克）也可轻微增强吗啡的抗伤害感受。这些结果表明，一氧化氮（NO）参与脊髓伤害感受事件，并且伤害性输入后NO产生的增加可能会降低脊髓中阿片类药物抗伤害感受的效率。
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