Breckwoldt W L, Genco C M, Connolly R J, Cleveland R J, Diehl J T
Department of Cardiothoracic Surgery, Tufts University School of Medicine, Boston, Massachusetts.
Ann Thorac Surg. 1991 Jun;51(6):959-63. doi: 10.1016/0003-4975(91)91015-n.
Spinal cord ischemia and resultant paraplegia are devastating sequelae in up to 40% of patients undergoing repair of thoracoabdominal aneurysms. We investigated the effect of intrathecal tetracaine on the neurological sequelae of spinal cord ischemia and reperfusion with aortic occlusion. Cocaine-derived anesthetics (lidocaine and its analogues) have been shown to decrease neuronal cell metabolism and also have specific neuronal membrane stabilizing effects. New Zealand white rabbits were anesthetized and spinal cord ischemia was then induced by infrarenal aortic occlusion. Animals were divided into six treatment groups. Tetracaine (groups 2 and 4) or normal saline solution (group 5) was administered intrathecally before aortic cross-clamping. Groups 1 and 3 functioned as controls. Group 6 animals received intravenous thiopental. Rabbits were classified as either neurologically normal or injured (paralyzed or paretic). Among controls, 25 minutes of aortic occlusion produced varied neurological sequelae (group 1, 3/6 injured, 50%) whereas 30 minutes resulted in more consistent injury (group 3, 5/6 injured, 83%). All rabbits that received intrathecal saline solution were paralyzed (group 5, 4/4 injured, 100%). Animals treated with intrathecal tetracaine and aortic occlusion of 30 minutes (group 4) showed significantly better preservation of neurological function (6/7 normal, 86%) than controls and saline-treated animals (groups 3 and 5). All animals treated with intrathecal tetracaine and aortic occlusion for 25 minutes (group 2) showed no signs of injury (5/5 normal, 100%), but this was not significant versus controls (group 1). Intravenous thiopental (group 6, 5/5 injured, 100%) had no beneficial effect. Intrathecal tetracaine significantly and dramatically abrogated the neurological injury secondary to spinal cord ischemia and reperfusion after aortic occlusion at 30 minutes in the rabbit model.
脊髓缺血及由此导致的截瘫是高达40%的胸腹主动脉瘤修复患者的灾难性后遗症。我们研究了鞘内注射丁卡因对脊髓缺血及主动脉阻断再灌注后神经后遗症的影响。可卡因衍生的麻醉剂(利多卡因及其类似物)已被证明可降低神经元细胞代谢,并且具有特定的神经元膜稳定作用。将新西兰白兔麻醉,然后通过肾下主动脉阻断诱导脊髓缺血。动物被分为六个治疗组。在主动脉交叉钳夹前鞘内注射丁卡因(第2组和第4组)或生理盐水(第5组)。第1组和第3组作为对照。第6组动物静脉注射硫喷妥钠。将兔子分为神经功能正常或受损(瘫痪或轻瘫)两类。在对照组中,25分钟的主动脉阻断产生了不同的神经后遗症(第1组,3/6受损,50%),而30分钟则导致更一致的损伤(第3组,5/6受损,83%)。所有接受鞘内生理盐水注射的兔子均瘫痪(第5组,4/4受损,100%)。接受鞘内丁卡因治疗且主动脉阻断30分钟的动物(第4组)显示神经功能的保存明显优于对照组和生理盐水治疗的动物(第3组和第5组)(6/7正常,86%)。所有接受鞘内丁卡因治疗且主动脉阻断25分钟的动物(第2组)均未出现损伤迹象(5/5正常,100%),但与对照组(第1组)相比无显著差异。静脉注射硫喷妥钠(第6组,5/5受损,100%)没有有益效果。在兔模型中,鞘内丁卡因显著且明显减轻了主动脉阻断30分钟后脊髓缺血及再灌注继发的神经损伤。