Spinella M, Bodnar R J
Department of Psychology, Queens College, City University of New York, Flushing 11367.
Pharmacol Biochem Behav. 1994 Mar;47(3):727-33. doi: 10.1016/0091-3057(94)90180-5.
Since nitric oxide (NO) has been implicated in nociceptive processing, the present study examined whether NO synthase inhibition with either Nw-nitro-L-arginine (L-NA) or its methyl ester (L-NAME) would alter antinociception elicited by either continuous (CCWS) or intermittent cold-water swims (ICWS) on the tail-flick and jump tests. Whereas CCWS antinociception on both tests was significantly potentiated by a dose range of L-NA (0.1-4 mg/kg IP) and L-NAME (1 mg/kg IP), ICWS antinociception was largely unaffected by these manipulations. In contrast, administration of the less active D isomer (D-NAME) failed to alter CCWS antinociception and reduced ICWS antinociception. The ability of NO synthase inhibition to potentiate CCWS antinociception could not be explained by changes in CCWS hypothermia. Since ICWS antinociception is mediated by mu-opioid manipulations and CCWS antinociception is sensitive to delta-opioid and nonopioid manipulations, this indicates that NO synthase inhibition may be acting upon a selective form of pain inhibition.
由于一氧化氮（NO）与伤害性感受处理有关，本研究考察了用Nω-硝基-L-精氨酸（L-NA）或其甲酯（L-NAME）抑制一氧化氮合酶是否会改变连续冷水游泳（CCWS）或间歇性冷水游泳（ICWS）在甩尾试验和跳跃试验中引发的镇痛作用。虽然在这两种试验中，一定剂量范围的L-NA（0.1 - 4mg/kg腹腔注射）和L-NAME（1mg/kg腹腔注射）能显著增强CCWS的镇痛作用，但ICWS的镇痛作用在很大程度上不受这些操作的影响。相比之下，活性较低的D-异构体（D-NAME）给药未能改变CCWS的镇痛作用，却降低了ICWS的镇痛作用。一氧化氮合酶抑制增强CCWS镇痛作用的能力无法用CCWS体温过低的变化来解释。由于ICWS的镇痛作用由μ-阿片类药物介导，而CCWS的镇痛作用对δ-阿片类药物和非阿片类药物操作敏感，这表明一氧化氮合酶抑制可能作用于一种选择性的疼痛抑制形式。
