| Objectve:The lamina of vertebra cutting is a common operation method in the spine surgery, however, the correlated research has not been reported about whether or not there is any influence as well as its degree to the spinal cord in the process of the lamina of vertebra cutting. In before experiments, the open spinal cord injury model was applicated in the research of the spinal cord injury which can't simulate the process of the lamina of vertebra cutting. On the base of the characters about the lamina of vertebra cutting, a closed spinal cord injury model is applicated. We applicate various load to the lamina and observe the influence of the impact load to the spinal cord, moreover, we try to find out the mechanisms of the influence and to observe the correlation between different observing index .Method:Normal 120 SD rats are divided randomly to 4 groups, each which includes 30 SD rats. A group is the control group which doesn't be impacted, when the abdominal cavity anesthesia succeed, the skin is cut and then close the notch. B, C and D group will be accepted the 10N, 15N and 20N outer lamina impacting load with the speed of 2m/s using a struck device, then the closed spinal cord injury model is established successfully.We choose randomly 6 rats in every group at different experimental time and then take different measures such as: BBB function score, SEP and MEP, the blood flow in the spinal cord central gray matter and the dorsum white matter, the blood pressure and the heart rate. Using the light microscope and the electron microscope we observe the spinal cord tissure. Making the spinal cord TUNEL labelling, and then we count the number of thepositive cells respectively in the gray matter and the white matter. In the end, we compare and analysis the experiment result between every group.Result:The influence of the spinal cord differs to various degree of the outer lamina impacting load.1 , Expect a temporary decrease of the gray matter blood flow at 0min, other observing index in B group and A group don't have any obvious difference. There isn't any obvious change of the blood pressure and HR in every group at different time.2, Motor function score in C and D group restore gradually after decreaseing, and the score in D group is lower than that of C group which restores quickly.3, The gray matter and white matter blood flow in C group decreases at 0min, and then increases gradually to normal in 24 days. In the D group, the blood flow decreases obviously at 0min and decreases continuously to the minimum in 6 hours, and then increases gradually but the flow is still remain under the normal value. The blood flow in D group is lower than that of C group at any time.4, There is no change of the SEP latent period in C group at Omin and 1h. It lengthens obviously at 1d and restores to normal on the whole in 12d. The amplitude of wave changes earlier than that of latent period, and it descends after 1h to the minimum after 1d and then restores gradually. There is no change of MEP latent period at Omin, and it lengthens in lh up to the most obvious at 1d and then restore gradually. The amplitude of wave descends at 0min and then descends gradually to the minimum in 1d, and then restores gradually. The latent period and amplitude of wave of SEP and MEP in D group begins to change at 0min, however, the phenomenon of the latent period lengthening and amplitude of wave descending at 1d indicates that perhaps there is reinjury, which restores gradually afterwards, but the latent period and the amplitude of wave are always lower than the numeric value at 0min.5, Through the histological observation in C group, we can find that the spinal cord structure is normal on the whole at Omin, and a small quantity of erythrocyte in the gray leak out at lh, also with a little edema, while the white matter doesn't change at all. At 6h,the erythrocyte's leaking reducess in the gray matter, the neur becomes hydropic degeneration, and the white matter becomes edema At 1d, the edema of gray matter take a turn for the better, and a part of neur degenerates obviously, however, we don't find necrosis zone, the white matter nerve fiber becomes slightly demyelination. The edema in the gray and white matter restore to normal at 12d and 24d.In D group, at 0min there are gray matter edema and erythrocyte exudation, the quantity of the bleeding erythrocyte in the gray matter increases at 1h, and the neur hydropic degeneration, the white matter becomes edema At 6h there is a small bleeding region in gray matte, the neur hydropic degeneration and the white matter becomes edema, the phenomenon of demyelination can be observed at local white matter. At 1d the bleeding region diminishes, while the edema is obvious and the nerve cells become necrosis, the phenomenon of demyelination can be observed at local region. At 6d the edema in gray begins to relieve, the small necrosis region can be found in the spinal central, the obvious edema and demyelination still exists in the white matter. At 12d and 24d, the edema in gray and white matter relieves obviously, but there is a small quantity of the nerve cell necrosis and demyelination.In C group, through the electron microscope we find that there are more apoptosis cells, and the chromatin pycnosis, the transparent vacuoles exists in the cell plasm but the cell membrane is integrity. At 12d and 24d there isn't obvious apoptosis cell. The necrosis cell isn't obvious at different time. The axis-cylinder is normal at Omin and lh. The shelf of myelin sheath at 6h is slightly confusion and its interspace enlarges slightly. At 1d, the delamination of the myelin sheath becomes seriously, and the nerve fiber becomes edema At 6d , the edema and the delamination of the myelin sheath relieves At 12d, the myelin sheath restores to normal.The necrosis nerve cells scattering in the gray and white matter can be found at 1h and 6h in D group, but it can be found rarely at other time. There are much more apoptosis cells at 6h and 1d, but the apoptosis cells aren't obvious in the gray matter at 12d and 24d when the apoptosis cells scattering in the white matter can be found. The axis-cylinder is normal at 0min, and the myelin sheath delamination is confusing at lh when the nerve fiberedema is obvious. The myelin sheath delamination becomes serious and a part structure of the axis-cylinder disappears at 6h. The edema becomes serious at 1d and a part of the axis-cylinder myelin sheath becomes thin and demyelination. The axis-cylinder edema relieves at 6h and it can be found demyelination partly. The phenomenon of the myelin sheath delamination relieves gradually at 12d and 24d.6, The number of the apoptosis nerve cell doesn't change in C group gray matter at 0min, and increases at 1h to the maximum at 1d. In the white matter, the number doesn't change at 0min and 1h, and the number increases at 6h to the maximum at 1d. The number in the gray and white matter doesn't increase obviously at 12d and 24d. The first time when the cells become apoptosis isn't coincident in the gray and white matter, and the time in the white matter is delaying.In the gray matter of the D group, the number doesn't change ay 0min,increase at 1h,get the maximum at 6h and 1d, then decrease.There is no increasing at 12d and 24d. In the white matter of the D group, the number doesn't change at Omin and 6h, and the number increases to the maximum at 6h and 1d, and then begins to decrease. Comparing with C group, the time of the peak is ahead of schedule, and the number is much more than C group and the time of the apoptosis is longer than C group. The apoptosis cells still scatter mainly in the white matter at 12d and 24d.7, Through the statistics analysis, we find that there is a linear correlation between the impacting load with some agents, such as the spinal cord blood flow change, the motor function, the evoked potential, and the number of the nerve cell apoptosis. The impacting load correlates obviously with the pathological changes of the spinal cord.Conclusion:The outer lamina impacting load can lead the spinal cord injury.With the outer lamina impacting load increaseing, the influence to the spinal cord will be more serious. If the impact load is 10N, there is not any change in the spinal cord. If the impacting load is 15N, the change in the spinal cord is reversible, and this change will recover in 24 days, so it is coincident with the standard of the spinal cord shock. If the impacting load is 20N, there is an obvious influence to the nerve function, and it will cause an lighter incompleteinjury to the spinal cord.The impacting injury to the spinal cord is mainly secondary injury , the primary injury ie minor.The outer lamina impacting load affects the spinal cord mainly through the alternation of the spinal cord microcirculation. There are two ways to alternate the spinal cord blood flow: one is the physiological change of the spinal cord microcirculation, another is the blood flow decreasing because of the microstructure destruction of the blood vessel. This impact load alternates much obviously the microcirculation blood flow of the gray matter.There is an obvious linear correlation between the change of spinal cord blood flow caused by the outer lamina impact load and the nerve cell apoptosis as well as the reinjury of the evoked potential. The phenomenon certificates that the spinal cord blood flow alternation caused by impact load is the capital reason of the secondary injury. It also certificates that the spinal cord blood flow plays an important role in the change of the nerve function.There is an obvious linear correlation between the outer lamina impact load and some aspects, such as the spinal cord blood flow, the motor function, the evoked potential and the pathological change. The motor evoked potential susceptibly reflects the change of the spinal cord ischemia after the impacting load. MEP is an important objective marker of the motor functional restoration, and it provides a safe operative monitoring to the impact load. We think it is safe when the amplitude descend in the 10% with the impacting load.
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