INVOLVEMENT OF NITRIC-OXIDE IN SPINALLY MEDIATED HYPERALGESIA IN THE MOUSE
INVOLVEMENT OF NITRIC-OXIDE IN SPINALLY MEDIATED HYPERALGESIA IN THE MOUSE
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DOI：
10.1016/0304-3940(92)90790-e
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发表时间：
1992-12-14
影响因子：
2.5
通讯作者：
WILCOX, GL
中科院分区：
文献类型：
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作者：
KITTO, KF;HALEY, JE;WILCOX, GL
鞘内注射n -甲基- d -天冬氨酸（NMDA）可引起小鼠短时间痛觉过敏。一氧化氮合酶（NOS）抑制剂N(omega)-硝基- l -精氨酸甲酯（L-NAME）通过全身或鞘内给药可阻断nmda诱导的痛觉过敏。这种作用被NOS底物l -精氨酸部分逆转。鞘内血红蛋白模拟了L-NAME的作用。鞘内注射no供体化合物硝普钠（SNP）和羟胺，导致痛觉过敏持续3小时，并通过共同给药血红蛋白减轻。因此，一氧化氮的产生似乎介导了nmda诱导的超敏反应，并可能导致其他形式的中枢性痛觉过敏。
Intrathecal injection of N-methyl-D-aspartate (NMDA) induces a short duration hyperalgesia in mice. An inhibitor of nitric oxide synthase (NOS), N(omega)-nitro-L-arginine methyl ester (L-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia. This effect was partially reversed by the NOS substrate, L-arginine. Intrathecal hemoglobin mimicked the effects Of L-NAME. Intrathecal injection of the NO-donating compounds, sodium nitroprusside (SNP) and hydroxylamine, resulted in a hyperalgesia that lasted 3 h and was reduced by coadministration of hemoglobin. Thus, nitric oxide production appears to mediate NMDA-induced hypersensitivity and may contribute to other forms of centrally induced hyperalgesia.