轴索的吗啡可能触发瞬态运动功能障碍后脊髓缺血的无害的间隔:临床和实验研究。
文章的细节
-
引用
复制到剪贴板 -
Kakinohana米、马沙拉白葡萄酒米,卡特C,戴维森JK, Yaksh TL
轴索的吗啡可能触发瞬态运动功能障碍后脊髓缺血的无害的间隔:临床和实验研究。
麻醉学。2003年4月,98 (4):862 - 70。
- PubMed ID
-
12657847 (在PubMed]
- 文摘
-
背景:胸腹的动脉瘤的病人进行了修复。硬膜外吗啡,4毫克,缓解疼痛。麻醉后病人显示下肢下肢轻瘫。这种效应被纳洛酮逆转。作者试图证明这些观察大鼠脊髓缺血模型定义鞘内吗啡管理的影响在不同时期回流后行为和脊髓组织病理学。方法:脊髓缺血诱导6分钟使用主动脉内气囊。吗啡或生理盐水,30 microg,鞘内注射为0.5,2,或者回流后24小时。在一个单独的组,脊髓缺血之前温度降低到27摄氏度。缺血后,恢复运动功能评估定期使用电动机赤字指数(0 =完全恢复;6 =完全截瘫)。 RESULTS: After ischemia, all rats showed near-complete recovery of function by 4-6 h. Intrathecal injection of morphine at 0.5 or 2 h of reflow (but not at 24 h) but not saline caused a development of hind limb dysfunction and lasted for 4.5 h (motor deficit index score = 4-6). This effect was reversed by intrathecal naloxone (30 microg). Intrathecal morphine administered after hypothermic ischemia was without effect. Histopathological analysis in animals that received intrathecal morphine at 0.5 or 2 h after ischemia (but not at 24 h) revealed dark-staining alpha motoneurons and interneurons. Intrathecal saline or spinal hypothermia plus morphine was without effect. CONCLUSIONS: These data indicate that during the immediate reflow following a noninjurious interval of spinal ischemia, intrathecal morphine potentiates motor dysfunction. Reversal by naloxone suggests that this effect results from an opioid receptor-mediated potentiation of a transient block of inhibitory neurons initiated by spinal ischemia.