CAJ | 학술논문

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48 h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5 min时SEPs P1潜伏期明显延长(P<0.01),P1波幅在缺血8 min时明显减小(P<0.01),缺血10 min时SEPs波形消失.再灌注后10 min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15 min时P1波幅恢复至缺血前(P<0.05).再灌注30 min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48 h P1波幅再次降低小于缺血前(P<0.01).再灌注24和48 h神经功能评分逐渐增加(P<0.01).再灌注24和48h P1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).冉灌注48 h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SEPs P1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.
목적 탐토척수결혈재관주손상중체감유발전위(SEPs)적변화규률급기대신경공능적감측작용.방법 26지신서란대백토채용신하복주동맥조단45min,건립척수결혈재관주모형.분별우결혈전、결혈5、8、10min급재관주10、15、30min、1、2、24화48h감측SEP변화.재관주24화48 h진행신경공능평분:재관주48h진행척수병이학관찰.결과 결혈5 min시SEPs P1잠복기명현연장(P<0.01),P1파폭재결혈8 min시명현감소(P<0.01),결혈10 min시SEPs파형소실.재관주후10 min시SEPs파형회복,단P1파폭소우결혈전(P<0.01),P1잠복기명현연장(P<0.01).재관주15 min시P1파폭회복지결혈전(P<0.05).재관주30 min후각시간점P1잠복기수연정회복추세,단잉명현연장(P<0.01);재관주24화48 h P1파폭재차강저소우결혈전(P<0.01).재관주24화48 h신경공능평분축점증가(P<0.01).재관주24화48h P1파폭변화여신경공능평분현저상관(r=-0.881화r=-0.925,P<0.01).염관주48 h가견수손척수발생출혈、수종、변성배사화중성립세포침윤.결론 척수결혈재관주손상중SEPs P1파폭변화교기잠복기경능준학지반영척수공능적손상정도,SEPs감측가이작위판단신경공능예후적가고지표.
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 (P<0.01) and the wave amplitude decreased 8 rain after ischemia (P<0.01). 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 (P<0.01). P1-wave amplitude became normal 15 min after the reperfusion (P>0.05), and the P1-wave latency gradually recovered 30 min alter reperfusion, but still significantly longer than the preisehemic value (P<0.01). P1-wave amplitude decreased again at 24 and 48 h alter reperfusion (P<0.01). The NFS gradually increased at 24 and 48 h fater the reperfusion (P<0.01). The changes in P1-wave amplitude at 24 and 48 h after reperfusion showed an obvious correlation toNFS (r=-0.881 and-0.925, respectively, P<0.01). 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.