Delayed neurological deterioration in the absence of direct spinal cord insult following
surgical decompression is a severe postoperative complication in patients with chronic severe
spinal cord compression (SCC). The
spinal cord ischemia-
reperfusion injury (IRI) has been verified as a potential etiology of the complication. However, the exact pathophysiologic mechanisms of the
decompression-related IRI remain to be defined. In this study, we developed a practical rat model of chronic severe SCC. To explore the underlying role of
inflammation in
decompression-related IRI, immunoreactivity of pro-inflammatory
cytokines including
tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) before and after
decompression were measured. In addition, expression level of TNF-α and IL-1β was examined with Western blot. Immunohistochemical staining showed negative result in gray matters in the
sham group and
sham-
decompression group. In the severe compression group, strong positive staining of TNF-α and IL-1β were found, suggesting a dramatic infiltration of inflammatory cells in gray matters. Furthermore, the severe compression group showed a significant increase in expression level of TNF-α and IL-1β as compared with the
sham group (p < 0.05). In the severe compression-
decompression group, both immunostaining and Western blot showed significant increase of TNF-α and IL-1β levels in the spinal cord compared with the severe compression group (p < 0.05). The results demonstrated that
surgical decompression plays a stimulative role in
inflammation through increasing the expression of inflammatory
cytokines in the rat model of chronic severe SCC injury.
Inflammation may be one of the important pathological mechanisms of
decompression-related IRI of chronic
ischemia.