Assessing the validity of a novel model of vertebral artery type of cervical syndrome induced by injecting sclerosing agent next to transverse process of cervical vertebra

Abstract

The efficacy of injecting sclerosing agent next to transverse process of cervical vertebra to induce vertebral artery type of cervical syndrome (CSA) was observed. Twenty rabbits were randomly divided into two groups: the model group and the control group. The rabbits in the model group were injected with sclerosing agent next to transverse process of cervical vertebray, on the contrary, the rabbits in the control group were injected with nothing. Transcranial Doppler (TCD) was used to detect the average speed of blood (Vm), pulsatility index (Pi) and the resistant index (Ri) of the vertebral artery, hematoxylin and eosin (HE) staining was used to observe the morphological changes, and immunohistochemistry was used to detect the expression of α-smooth muscle actin (α-SMA) and matrix metalloproteinase-2(MMP-2). TCD showed increased Pi, Ri and decreased Vm in the model group (P<0.05) compared with the control group. HE staining revealed hyperplasia and hypertrophied smooth muscle cells in the model group (P<0.05). Immunohistochemistry displayed up-regulation of α-SMA and MMP-2 in the model group (P<0.05). It was concluded that injecting sclerosing agent next to transverse process of cervical vertebra induces remodeling of vertebral artery in rabbits, suggesting it is a practical method to establish CSA animal model.

Keywords

vertebral artery / cervical syndrome / animal model

References

[1] ZhuM.S., ZhengZ., HuangY., et al.. Using sclerosing agent injection method to make rabbit model of vertebra arterial cervical spondylosis. Zhong Yi Zheng Gu (Chinese), 2000, 12(12): 11-13

[2] WangY.J., ShiQ., LuW.W., et al.. Cervical intervertebral disc degeneration induced by unbalanced dynamic and static forces: a novel in vivo rat model. Spine, 2006, 31(14): 1532-1538

[3] HendersonF.C., GeddesJ.F., VaccaroA.R., et al.. Stretch-associated injury in cervical spondylotic myelopathy: new concept and review. Neurosurgery, 2005, 56(5): 1101-1113

[4] TeixeiraL.R., VargasF.S., AcencioM.M., et al.. Influence of parecoxib (cox-2 inhibitor) in experimental pleurodesis. Respir Med, 2009, 103(4): 595-600

[5] DemircanM.N., AsirA., CetinkalA., et al.. Is there any relationship between proinflammatory mediator levels in disc material and myelopathy with cervical disc herniation and spondylosis? A non-randomized, prospective clinical study. Eur Spine J, 2007, 16(7): 983-986

[6] TachiharaH., KikuchiS., KonnoS., et al.. Does facet joint inflammation induce radiculopathy? an investigation using a rat model of lumbar facet joint inflammation. Spine, 2007, 32(4): 406-412

[7] YuT.B., XiaY.J., ZhouB.W.. The effect of sympathetic factor on the blood flow of vertebral-basal artery. Zhongguo Jizhu Yu Jisui Zazhi (Chinese), 2000, 10(3): 157-159

[8] HaskóG.. Receptor-mediated interaction between the sympathetic nervous system and immune system in inflammation. Neurochem Res, 2001, 26(8–9): 1039-1044

[9] Rodríguez-MañasL., El-AssarM., VallejoS., et al.. Endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation. Aging Cell, 2009, 8(3): 226-238

[10] TatenkulovaS.N., MareevV., ZykovK.A., et al.. The role of inflammatory factors in pathogenesis of ischemic heart disease. Kardiologiia, 2009, 49(1): 4-8

[11] DonatoA.J., GanoL.B., EskurzaI., et al.. Vascular endothelial dysfunction with aging: endothelin-1 and endothelial nitric oxide synthase. Am J Physiol Heart Circ Physiol, 2009, 297(1): H425-H432

[12] JiaoL., WangM.C., YangY.A., et al.. Norepinephrine reversibly regulates the proliferation and phenotypic transformation of vascular smooth muscle cells. Exp Mol Pathol, 2008, 85(3): 196-200

[13] JohnsonR., WebbJ.G., NewmanW.H., et al.. Regulation of human vascular smooth muscle cell migration by beta-adrenergic receptors. Am Surg, 2006, 72(1): 51-54

[14] BleekeT., ZhangH., MadamanchiN., et al.. Catecholamine-induced vascular wall growth is dependent on generation of reactive oxygen species. Circ Res, 2004, 94(1): 37-45

[15] AnggrahiniD.W., EmotoN., NakayamaK., et al.. Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation. Cardiovasc Res, 2009, 82(1): 143-151

[16] SoliniA., SantiniE., MadecS., et al.. Effects of endothelin-1 on fibroblasts from type 2 diabetic patients: Possible role in wound healing and tissue repair. Growth Factors, 2007, 25(6): 392-399

[17] MiyakeT., AokiM., MorishitaR., et al.. Inhibition of anastomotic intimal hyperplasia using a chimeric decoy strategy against NF-kappaB and E2F in a rabbit model. Cardiovasc Res, 2008, 79(4): 706-714

[18] KurokawaK., SakiyamaK., AbeS., et al.. Expression of myosin heavy-chain mRNA in cultured myoblasts induced by centrifugal force. Bull Tokyo Dent Coll, 2008, 49(4): 179-184

[19] ChiangH.Y., KorshunovV.A., SerourA., et al.. Fibronectin is an important regulator of flow-induced vascular remodeling. Arterioscler Thromb Vasc Biol, 2009, 29(7): 1074-1079

[20] AmbalavananN., NicolaT., LiP., et al.. Role of matrix metalloproteinase-2 in newborn mouse lungs under hypoxic conditions. Pediatr Res, 2008, 63: 26-32

[21] ZouY., QiY., RoztocilE., et al.. Patterns of gelatinase activation induced by injury in the murine femoral artery. J Surg Res, 2009, 154(1): 135-142

[22] YangE.V., SoodA.K., ChenM., et al.. Norepinephrine up-regulates the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumor cells. Cancer Res, 2006, 66(21): 10 357-10 364

[23] MenonB., SinghM., SinghK.. Matrix metalloproteinases mediate beta-adrenergic receptor-stimulated apoptosis in adult rat ventricular myocytes. Am J Physiol Cell Physiol, 2005, 289(1): C168-C176

[24] SpiegelA., ShivtielS., KalinkovichA., et al.. Catecholaminergic neurotransmitters regulate migration and repopulation of immature humanCD34⁺ cells through Wnt signaling. Nat Immunol, 2007, 8(10): 1123-1131

[25] MurrayD.B., McMillanR., BrowerG.L., et al.. ETA selective receptor antagonism prevents ventricular remodeling in volume overloaded rats. Am J Physiol Heart Circ Physiol, 2009, 297(1): H109-H116