The Exacerbating Effects of Intrathecal Morphin on Neurological Outcome after Non-Injurious Interval of Spinal Cord Ischemia in The Rat.

为探讨鞘内注射吗啡（IT）对脊髓缺血的加重作用，采用大鼠脊髓缺血模型，进行了神经功能学、脊髓组织病理学和脑脊液微透析研究。重复鞘内注射30 μg吗啡（30M组）导致痉挛逐渐发展，站立、行走或行走能力几乎完全丧失。这些动物在再灌注72小时期间表现出不可逆的运动缺陷。注射30 μg吗啡可引起痉挛性截瘫，而注射10 μ g或3 μg吗啡则不能引起痉挛性截瘫。微透析研究表明，鞘内注射吗啡再灌注8h后，脑脊液谷氨酸含量显著升高，提示主动脉阻断后，吗啡作用于脊髓，可诱发痉挛性截瘫，并可能造成不可逆的脊髓损伤而导致截瘫。

To investigate the exacerbating effects of intrathecal (IT) morphine administration after short lasting spinal cord ischemia, neurological outcome, histopathological analysis of spinal cord and microdyalysis study in CSF were carried out using the spinal ischemia model in rats. Repetitive-intrathecal injection of 30 μg of morphine (group 30M) resulted in a gradual development of spasticity and a near complete loss of the ability to stand, walk or step. These animals displayed the irreversible motor deficit during 72 hours of reperfusion. The morphine induced spastic paraplegia could be caused only by IT 30 μg of morphine, but not by 10 or 3 μg of morphine. Microdyalysis study showed the significant increase of the CSF-glutamate level following intrathecal injection of morphine for 8 hours of reperfusion.These results suggested that, when morphine affect on the spinal cord after short lasting of aortic occlusion, spastic paraplegia could be induced and this might cause irreversible injury of spinal cord leading to paraplegia.