持续脊髓压迫:第二部分:甲基强的松龙对局部血流和体感诱发电位恢复的影响

G. Carlson, C. Gorden, S. Nakazawa, E. Wada, Jeremy S. Smith, J. LaManna
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引用次数: 34

摘要

背景:甲基强的松龙治疗外伤性脊髓损伤的疗效存在争议。我们检查了甲基强的松龙对局部脊髓血流的影响,并试图确定电生理功能的恢复是否依赖于再灌注,无论是在持续脊髓压迫期间还是在减压后。方法:采用犬脊髓动态受压模型,观察甲基强的松龙治疗对体感诱发电位恢复和脊髓血流的影响。在停止脊髓动态压迫和所有体感诱发电位丧失后5分钟,对36只比格犬(每组18只)给予甲基强龙(30mg /kg静脉负荷剂量,然后静脉滴注5.4 mg/kg/hr)或生理盐水溶液。持续压迫90分钟后,脊髓被减压。在持续压迫期间和减压后3小时评估体感诱发电位和脊髓血流量。结果:7只接受甲基强的松龙治疗的狗在持续压迫过程中恢复了可测量的体感诱发电位,而没有一只接受生理盐水治疗的狗。减压后,3只接受甲基强的松龙治疗的狗和7只接受生理盐水治疗的狗恢复了体感诱发电位。4只接受甲基强的松龙治疗的狗失去了先前可测量的体感诱发电位。在甲基强的松龙组,恢复体感诱发电位的狗的脊髓血流量显著高于未恢复体感诱发电位的狗(p < 0.05)。盐水组再灌注血流量显著高于甲基强的松龙组(p < 0.05)。盐水组脊髓血流量在减压后5分钟内恢复到基线水平。接受甲基强的松龙治疗的狗没有恢复到基线水平。结论:本研究中使用的甲基强的松龙在神经保护或恢复方面没有提供大的或显著的持久益处。甲基强的松龙可能通过影响正常的自我调节血流功能的机制减少脊髓局部血流量。临床相关性:这项研究表明甲基强的松龙治疗的一个主要缺点可能是减压后脊髓局部血流量的减少。
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Sustained Spinal Cord Compression: Part II: Effect of Methylprednisolone on Regional Blood Flow and Recovery of Somatosensory Evoked Potentials
Background: The efficacy of methylprednisolone in the treatment of traumatic spinal cord injury is controversial. We examined the effect of methylprednisolone on regional spinal cord blood flow and attempted to determine whether recovery of electrophysiological function is dependent on reperfusion, either during sustained spinal cord compression or after decompression.Methods: The effects of methylprednisolone therapy on recovery of somatosensory evoked potentials and on spinal cord blood flow were examined in a canine model of dynamic spinal cord compression. Methylprednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered to thirty-six beagles (eighteen in each group) five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. Somatosensory evoked potentials and spinal cord blood flow were evaluated throughout the period of sustained compression and for three hours after decompression.Results: Seven dogs treated with methylprednisolone and none treated with saline solution recovered measurable somatosensory evoked potentials during sustained compression. After decompression, three more dogs treated with methylprednisolone and seven dogs treated with saline solution recovered somatosensory evoked potentials. Four dogs treated with methylprednisolone lost their previously measurable somatosensory evoked potentials. In the methylprednisolone group, spinal cord blood flow was significantly higher (p < 0.05) in the dogs that had recovered somatosensory evoked potentials than it was in the dogs that had not. Reperfusion blood flow was significantly higher (p < 0.05) in the saline-solution group than it was in the methylprednisolone group. Spinal cord blood flow in the saline-solution group returned to baseline levels within five minutes after decompression. It did not return to baseline levels in the dogs treated with methylprednisolone.Conclusions: The methylprednisolone administered in this study did not provide a large or significant lasting benefit with regard to neurological preservation or restoration. Methylprednisolone may reduce regional spinal cord blood flow through mechanisms affecting normal autoregulatory blood-flow function.Clinical Relevance: This study suggests that a major drawback of methylprednisolone therapy may be the reduction in regional spinal cord blood flow after decompression.
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