Jellish Walter S, Zhang Xin, Langen Kenneth E, Spector Matthew S, Scalfani Michael T, White Fletcher A
Department of Anesthesiology, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Anesthesiology. 2008 Jan;108(1):78-86. doi: 10.1097/01.anes.0000296109.04010.82.
In this study, the authors determined the effect of magnesium sulfate on intrathecal glutamate concentrations, hindlimb motor function, and histopathology after a transient episode of spinal cord ischemia.
Fifty-two New Zealand White rabbits underwent spinal cord ischemia for 30 min. Fifteen minutes before ischemia, animals received intrathecal magnesium sulfate (MgSO4) (3 mg/kg) or placebo (artificial cerebrospinal fluid). Intrathecal microdialysis samples were measured for glutamate using high-performance liquid chromatography. Neurologic function and spinal cord histopathology were assessed throughout the recovery period.
Intrathecal glutamate levels in placebo-treated animals were higher after spinal cord ischemia compared with sham- and MgSO4-treated animals. MgSO4-treated animals had increased lower extremity motor function compared with the placebo group (64.7% vs 14.3%, P < 0.01). Histologic examination of placebo-treated animals revealed significant motor neuron cell loss at thoracolumbar levels by Day 7 (P < 0.05), whereas lower lumbar regions displayed significant neuron loss on Day 1. Spinal cords from MgSO4-treated animals exhibited less neuronal loss in lumbar regions. Similar effects were present in the thoracolumbar segments on Day 7. A significant correlation existed between diminished neuronal loss and hind leg movement (Tarlov score) and demonstrates that the neurologic outcome after MgSO4 treatment was related to lower lumbar ventral horn cell survival (r2 = 0.812, P < 0.001).
These results demonstrate that MgSO4 affords significant spinal cord motor neuron protection by diminishing acute neuronal loss at the foci of the ischemic injury (L3-L6) with delayed neuronal degeneration in adjacent spinal cord regions (T7-L2).
在本研究中，作者确定了硫酸镁对脊髓短暂缺血后鞘内谷氨酸浓度、后肢运动功能和组织病理学的影响。
52只新西兰白兔经历30分钟的脊髓缺血。在缺血前15分钟，动物接受鞘内硫酸镁（MgSO4）（3mg/kg）或安慰剂（人工脑脊液）。使用高效液相色谱法测量鞘内微透析样本中的谷氨酸。在整个恢复期评估神经功能和脊髓组织病理学。
与假手术组和硫酸镁治疗组动物相比，脊髓缺血后接受安慰剂治疗的动物鞘内谷氨酸水平更高。与安慰剂组相比，硫酸镁治疗组动物的下肢运动功能有所改善（64.7%对14.3%，P<0.01）。对接受安慰剂治疗的动物进行组织学检查发现，到第7天胸腰段出现明显的运动神经元细胞丢失（P<0.05），而在第1天腰下段出现明显的神经元丢失。硫酸镁治疗组动物的脊髓在腰段显示出较少的神经元丢失。在第7天胸腰段也有类似的效果。神经元丢失减少与后腿运动（Tarlov评分）之间存在显著相关性，表明硫酸镁治疗后的神经学结果与腰下段腹侧角细胞存活有关（r2 = 0.812，P<0.001）。
这些结果表明，硫酸镁通过减少缺血性损伤灶（L3-L6）处的急性神经元丢失以及相邻脊髓区域（T7-L2）的延迟神经元变性，为脊髓运动神经元提供了显著的保护。
