Article
Vascular and metabolic changes in canine dorsal root ganglia undergoing nerve root compression
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Published: | September 14, 2016 |
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Outline
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Lumbosacral neuroforaminal stenosis (LNFS) is a common cause of sciatica in people and large breed dogs. Nerve root entrapment goes with significant swelling of the tissue, which winds-up the pressure on the root in a vicious circle. Thereby, compression of small vessels is supposed to increase vascular resistance of the dorsal root ganglion (DRG) causing malperfusion and metabolic derangement of sensory neurons. In order to elucidate the vascular-haemodynamic hypothesis behind rhizopathic pain, this study addressed the impact of LNFS on DRG vascularity and metabolic stress.
15 L7-DRG were harvested from dogs suffering from recrudescent pain due to LNFS, non-responsive to conventional analgesics. The investigation enrolled blood vessel density and distribution as well as their histomorphology. Furthermore, the immunohistochemical expression of vascular endothelial growth factor (VEGF), neuroglobin (NGB), carbonic anhydrase IX (CA-IX), monocarboxylate transporter-1 (MCT-1) and -4 (MCT-4) was assessed.
On stereological analysis, there was no difference of vascular density in between affected DRG and control tissues, whereas 50% of LNFS samples showed histological abnormalities, comprising thickened arterial walls, endothelial prominence and phlebectasia. Furthermore in LNFS cases VEGF expression was significantly increased in neurons, satellite cells and endothelial cells. Neurons and satellite cells showed significantly higher immunoreactivity (p<0.05) for, CA-IX, MCT-1, MCT-4 while NGB was significantly increased in satellite cells only.
Canine NFS is characterized by prolonged hypoxic conditions leading to vascular and metabolic changes within the DRG. A shift towards glycolytic metabolism and prevention of an acidotic environment was identified through increased expression of CA-IX and MCTs. Increased expression of hypoxia markers VEGF and NGB is further indicative of adaptive mechanisms countering hypoxic stress that is likely to contribute to neuropathic pain in sciatica.