RESUMEN
Objective To explore the establishment of animal models of incomplete spinal cord ischemic injury to provide ideal carriers for researching the pathogenesis of incomplete spinal cord ischemic injury.Methods Twenty-four New Zealand rabbits were randomly divided into a control group (n=8) and 2 experimental groups (n=16); control group only underwent sham-operation without inducing spinal cord injury to exclude the influences of anesthesia and surgery on motor evoked potential (MEP); in the experimental groups,spinal cord ischemia injury models were established by the methods of selective ligation of segmental spinal artery from cranio-caudal direction.Baseline MEP after anesthetization were recorded,and the MEP 30 min,2 and 7 d after vascular ligation were noted.Motor function was assessed after narcotic conscious,and 2 and 7 d after vascular ligation.The specimens 7 d after ligation were taken for HE staining.Results The amplitude of MEP in the experimental group having 3 lumbar artery ligation 30 minutes after ligation was significantly different as compared with that in the control group (P＜0.05); no significant differences on the amplitude of MEP were noted between these 2 groups 2 and 7 d after ligation (P＞0.05).Significant differences on the amplitude of MEP were noted between control group and experimental group having 4 lumbar artery ligation 30 min,and 2 and 7 d after ligation (P＜0.05).The latency of all these rabbits showed no significant difference 30 min,and 2 and 7 d after ligation (P＞0.05).The amplitude changes of MEP were accorded with the results of motor function scale.Conclusion Reversible incomplete spinal cord ischemia animal models can be established after 3 lumbar artery ligation; irreversible incomplete spinal cord ischemia animal models can be established after 4 lumbar artery ligation.
RESUMEN
Objective To provide the theoretical basis for the application of cortical somatosensory evoked potential (CSEP) in monitoring the function of the spinal cord to prevent postoperative neurological dysfunction. Methods Thirty-three New Zealand rabbits were randomly divided into 6 groups: 8 were chosen as control group to eliminate the influence of anesthesia and surgery on the evoked potential; the other 25 were assigned to 5 sub-experimental groups (n=5) according to the artery number being ligatured in the left renal arteries and the spinal arteries. Baseline evoked potential in each group was noted immediately after anesthesia; the CSEP were recorded at different time points (before vascular ligation, 30 min and 2 d after vascular ligation). Motor functions were assessed after narcotic conscious and 2 d after vascular ligation. The specimens were taken for HE staining. Results The latency was not sensitive to spinal cord ischemia and no significant difference of that was found between the experimental groups and the control group (P>0.05); except that, the changes of theamplitudes were very complex and the specificity of motor function was decreased. The amplitude reduced and then gradually restored in the 2, 3 and 4 levels of ligation. The changes of amplitude could indicate the degree of pathological damage in the spinal cord and its motor function. Conclusion Complex amplitude of somatosensory evoked potential can be found in the acute phase of ischemia in the spinal cord. Specificity of motor function is poor resulting from its signal averaging process. Motor evoked potential monitoring in the operation should also be added in the detection of the spinal cord.