体感诱发电位监测脊髓缺血再灌注损伤的实验研究

Somatosensory-evoked potential monitoring for evaluation of spinal cord ischemia-reperfusion injury in rabbits

目的探讨脊髓缺血再灌注损伤中体感诱发电位(SEPs)的变化规律及其对神经功能的监测作用。方法26只新西兰大白兔采用肾下腹主动脉阻断45min,建立脊髓缺血再灌注模型。分别于缺血前、缺血5、8、10min及再灌注10、15、30min、1、2、24和48h监测SEP变化。再灌注24和48h进行神经功能评分;再灌注48h进行脊髓病理学观察。结果缺血5min时SEPsP1潜伏期明显延长(P<0.01),P1波幅在缺血8min时明显减小(P<0.01),缺血10min时SEPs波形消失。再灌注后10min时SEPs波形恢复,但P1波幅小于缺血前(P<0.01),P1潜伏期明显延长(P<0.01)。再灌注15min时P1波幅恢复至缺血前(P>0.05)。再灌注30min后各时间点P1潜伏期虽然呈恢复趋势,但仍明显延长(P<0.01);再灌注24和48hP1波幅再次降低小于缺血前(P<0.01)。再灌注24和48h神经功能评分逐渐增加(P<0.01)。再灌注24和48hP1波幅变化与神经功能评分显著相关(r=-0.881和r=-0.925,P<0.01)。再灌注48h可见受损脊髓发生出血、水肿、变性坏死和中性粒细胞浸润。结论脊髓缺血再灌注损伤中SEPsP1波幅变化较其潜伏期更能准确地反映脊髓功能的损伤程度,SEPs监测可以作为判断神经功能预后的可靠指标。

Objective To assess the changes of somatosensory evoked potentials （SEPs） during spinal cord ischemia and reperfusion injury and the value of SEP monitoring in evaluating neurological functions in this setting. Methods Spinal cord ischemia-reperfusion injury was induced in 28 rabbits by clamping the infrarenal aorta for 45 min, and the SEPs were monitored before and at 5, 10, and 15 min after ischemia, and at 15, 30, and 60 min and 2, 24 and 48 h after reperfusion. The neurological function score （NFS） of the rabbits was evaluated at 6, 12, 24 and 48 h after reperfusion, and the pathological changes of the spinal cord were observed 48 h after reperfusion. Results SEPs P1-wave latency significantly increased 5 min after ischemia （P0.01） and the wave amplitude decreased 8 min after ischemia （P0.01）. SEPs disappeared 10 min after ischemia and recovered 15 min after reperfusion, but the P1-wave latency still remained longer and P1-wave amplitude lower than the measurements before ischemia （P0.01）. P1-wave amplitude became normal 15 min after the reperfusion （P0.05）, and the P1-wave latency gradually recovered 30 min after reperfusion, but still significantly longer than the preischemic value （P0.01）. P1-wave amplitude decreased again at 24 and 48 h after reperfusion （P0.01）. The NFS gradually increased at 24 and 48 h fater the reperfusion （P0.01）. The changes in P1-wave amplitude at 24 and 48 h after reperfusion showed an obvious correlation to NFS （r=-0.881 and -0.925, respectively, P0.01）. Hemorrhage, swelling, and degeneration and neutrophil infiltration occurred in the spinal cord tissue 48 h after the reperfusion. Conclusion The changes of SEP P1-wave amplitude can better reflect the spinal cord function than the wave latency during spinal cord ischemia-reperfusion injury, and SEP monitoring provides reliable evidence for prognostic evaluation of the neurological function.