Viscoelastic relaxation and regional blood flow response to spinal cord compression and decompression
Viscoelastic relaxation and regional blood flow response to spinal cord compression and decompression
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DOI：
10.1097/00007632-199706150-00002
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发表时间：
1997-06-15
期刊：
影响因子：
3
通讯作者：
LaManna, JC
中科院分区：
文献类型：
--
作者：
Carlson, GD;Warden, KE;LaManna, JC
研究设计。为了更好地了解脊髓损伤的主要力学因素与继发性损伤机制之间的关系，本研究在控制脊髓速度位移和实时活塞-脊髓界面压力反馈的犬体内模型中评估了区域血流和体感诱发电位功能。目的：探讨脊髓局部血流和粘弹性松弛对脊髓减压和不减压时神经传导恢复的影响。背景资料摘要。机械因素和血管因素在脊髓损伤中的相对作用尚未明确。12只小猎犬麻醉后行T13椎板切除术。采用液压加载活塞对脊髓进行等速压缩，并将微型压力传感器固定在脊柱上。当体感诱发电位幅度下降50%（最大压缩）时，脊髓位移停止。6只动物在最大压迫5分钟后进行减压，并与6只脊髓移位维持3小时未减压的动物进行比较，用荧光微球技术测量脊髓局部血流量。在最大压缩时，损伤部位脊髓局部窝流量由19.0 +/- 1.3 mL/ 100g /min降至12.6 +/- 1.0 mL/ 100g /min，而活塞-脊髓界面压力为30.5 +/- 1.8 kPa，脊髓位移为2.1 +/- 0.1 mm（平均+/- SE）。活塞停止平移5 min后，脊髓界面压力减弱51%，体感诱发电位振幅继续下降至基线的16%。持续压缩组，脊髓界面压力在90分钟内松弛至最大压力的13%；然而，体感诱发电位功能没有恢复，在最大压迫后30分钟和180分钟，局部脊髓血流量仍明显低于基线。在6只接受脊髓减压的动物中，体感诱发电位功能和脊髓局部血流量在最大压力30分钟后恢复到基线水平。尽管在最大压迫后5分钟内脊髓迅速松弛超过50%，但只有在早期减压后才恢复体感诱发电位传导。脊髓减压与局部尖晶石血流量的早期恢复和体感诱发电位的恢复有关。到3小时时，受压组和减压组的脊髓血流量相似，尽管只有减压组出现体感诱发电位恢复。
Study Design. To better understand the relationships between primary mechanical factors of spinal cord trauma and secondary mechanisms of injury, this study evaluated regional blood flow and somatosensory evoked potential function in an in vivo canine model with controlled velocity spinal cord displacement and real-time piston-spinal cord interface pressure feedback.Objectives. To determine the effect of regional spinal cord blood flow and viscoelastic cord relaxation on recovery of neural conduction, with and without spinal cord decompression.Summary of Background Data. The relative contribution of mechanical and Vascular factors on spinal cord injury remains undefined.Methods. Twelve beagles were anesthetized and underwent T13 laminectomy. A constant velocity spinal cord compression was applied using a hydraulic loading piston with a subminiature pressure transducer rigidly attached to the spinal column. Spinal cord displacement was stopped when somatosensory evoked potential amplitudes decreased by 50% (maximum compression). Six animals were decompressed 5 minutes after maximum compression and were compared with six animals who had spinal cord displacement maintained for 3 hours and were not decompressed, Regional spinal cord blood flow was measured with a fluorescent microsphere technique.Results. At maximum compression, regional spinal cord brood flow at the injury site fell from 19.0 +/- 1.3 mL/100 g/min to 12.6 +/- 1.0 mL/100 g/min, whereas piston-spinal cord interface pressure was 30.5 +/- 1.8 kPa, and cord displacement measured 2.1 +/- 0.1 mm (mean +/- SE), Five minutes after the piston translation was stopped, the spinal cord interface pressure had dissipated 51%, whereas the somatosensory evoked potential amplitudes continued to decrease to 16% of baseline. In the sustained compression group, cord interface pressure relaxed to 13% of maximum within 90 minutes; however, no recovery of somatosensory evoked potential function occurred, and regional spinal cord blood flow remained significantly lower than baseline at 30 and 180 minutes after maximum compression. in the six animals that underwent spinal cord decompression, somatosensory evoked potential function and regional spinal cord blood flow recovered to baseline 30 minutes after maximum compression.Conclusions. Despite rapid cord relaxation of more than 50% within 5 minutes after maximum compression, somatosensory evoked potential conduction recovered only with early decompression. Spinal cord decompression was associated with an early recovery of regional spinel cord blood flow and somatosensory evoked potential recovery. By 3 hours, spinal cord blood flow was similar in both the compressed and decompressed groups, despite that somatosensory evoked potential recovery occurred only in the decompressed group.