Damage control orthopedics for spinal cord compression injury in rabbits

English Keywords:Spinal cord injury  Matrix metallopeptidase-2  Apoptosis  Flow cytometry  Damage control operation

English Abstract:

  【Abstract】 Objectives: To investigate the operation procedures and outcomes of damage control operation for spinal cord compression injury in rabbits. Methods: The animal models of spinal cord compression injury were established by balloon compression in 45 white New Zealand rabbits. Decompression began 2 days after the first operation. 5 rabbits were randomly selected from the 45 models to carry on the following researches two hours after operation(control group): behavioral science, apoptotic spinal cord cells detected by flow cytometry, and expression of matrix metallopeptidase-2(MMP-2) detected by histopathological and immunohistochemical staining. The remaining 40 rabbits were randomly divided into 2 groups, 20 cases in each group. In the first group, the total laminectomy began far from the heavy oppressed side of spinal cord after balloon pressure reduced to half(contralateral decompression group, group A). In the second group, the whole vertebral plate was resected from the heavily oppressed side(ipsilateral decompression group, group B). Then the balloons were took out after decompression in the 2 groups. 5 rabbits were randomly and respectively taken from the 2 groups at 1d, 3d, 7d, 14d after decompression to complete the above test contents. Results: The differences of improved Tarlov motor function grades were not statistically significant between control group and group A or B at 1d after decompression(P>0.05). The differences of improved Tarlov motor function grades were not statistically significant between group A and B at 1d, 3d, 7d of post-decompression(P>0.05).　The improved Tarlov motor function grade test in group A was significantly improved compared with that in group B at 14d after decompression(P<0.05). No significant difference was found with respect to the apoptosis between group A and B(P>0.05) at 1d, 3d after decompression. The apoptosis was lower in group A and B at 1d of post-decompression than control group(P<0.05). The difference of the apoptosis was not statistically significant between 1d and 3d of post-decompression and between 7d and 14d of post-decompression in group A(P>0.05) and the same as in group B(P>0.05). However, the apoptosis was higher at 7d than at 3d post-decompression in group A(P<0.05) and the same as in group B(P<0.05). In addition, the apoptosis was lower in group A than group B at 7d and 14d after decompression(P<0.05). HE staining in control group showed mild demyelination changes and vacuolar degeneration in white matter company with nerve cell edema and neuron atrophy in gray matter. The injury of spinal cord at 1d, 3d, 7d and 14d after decompression in group A and B showed nerve cell edema company with degeneration in gray matter until pathological changes deteriorated at 7d after decompression, and maintained the changes to 14d after decompression. The diffuse demyelination changes company with dotted hemorrhage was showed in white matter. The immunohistochemical staining method to detect expression of MMP-2 in rabbits showed that the expression of MMP-2 in group B was significantly higher than that in group A(P<0.05). The expression of MMP-2 was lower in group A and B at 1d of post-decompression than in contol group(P<0.05). The expression of MMP-2 was higher at 3d than that in 7d of post-decompression and the expression was higher at 7d than that at 14d of post-decompression in group A and the same as in group B(P<0.05). However, no significant difference was found with respect to the expression of MMP-2 between 1d and 3d of post-decompression in group A(P>0.05) and the same as in group B(P>0.05). Conclusions: Ipsilateral decompression decompresses from the heavy oppressed side of spinal cord without increasing the effective volume of spinal canal, which easily causes the second spinal cord injury. Damage control operation is more effective than ipsilateral decompression in thoracolumbar burst fracture that causes spinal cord oppression and injury.