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以钾离子透入引起大鼠甩尾的电流强度 ( m A)作为痛反应指标 ,采用侧脑室微量注射 L-精氨酸 ( L-Arg)、亚甲基蓝 ( MB)等 ,观察大鼠痛阈的变化 ,分析探讨中枢神经系统中一氧化氮 ( NO)对大鼠痛觉的调制作用。结果显示 :大鼠侧脑室微量注射 NO前体及供体物质 L- Arg和硝普钠 ( SNP)均引起明显的痛敏效应。微量注射 MB和 L- NAME后大鼠痛阈升高非常显著。侧脑室微量注射 MB和 L - Arg混合液后 ,大鼠痛阈较单纯注射 MB组表现出明显降低的趋势 ,但与 L- Arg组相比大鼠痛阈升高明显。提示 :提高中枢内 NO水平具有明显的痛敏效应 ,而降低中枢神经系统 NO水平表现显著镇痛作用。中枢神经系统 NO对大鼠痛觉的调制作用至少部分是通过 NO- c GMP途径实现的。
The current intensity (m A) of tail-flicking rats induced by potassium ion was used as the index of pain reaction. L-arginine (L-Arg) and methylene blue (MB) were injected into the lateral ventricle to observe the pain threshold Changes, analysis of central nervous system nitric oxide (NO) modulation of rat pain sensation. The results showed that microinjection of NO precursor into the lateral ventricle and the donor substance of L-Arg and SNP all induced obvious hyperalgesia. Increased pain threshold in rats after microinjection of MB and L-NAME. After intracerebroventricular injection of MB and L - Arg mixture, the pain threshold of rats was significantly decreased compared with MB group, but the pain threshold of rats increased significantly compared with L - Arg group. Tip: to improve the central NO level has a significant pain-sensitive effect, and reduce the central nervous system NO level showed significant analgesic effect. The modulatory effect of central nervous system NO on the pain sensation in rats is achieved at least in part by the NO-c GMP pathway.