Inhibition of neurogenic inflammation as a novel treatment for ischemic stroke

Drug News and Perspectives

Volumn 20, Issue 4, 2007, Pages 221-226

  Turner, Renée ^a   Vink, Robert ^a,b  

^a UNIVERSITY OF ADELAIDE   (Australia)

^b HANSON INSTITUTE   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

BARBITURIC ACID DERIVATIVE; CAPSAICIN; CORTICOSTEROID; MANNITOL; NEUROPEPTIDE; NOLPITANTIUM; SUBSTANCE P; TISSUE PLASMINOGEN ACTIVATOR;

BLOOD BRAIN BARRIER; BRAIN EDEMA; CELL DEATH; CEREBROSPINAL FLUID; CEREBROVASCULAR ACCIDENT; DISEASE ASSOCIATION; DISEASE COURSE; DRUG EFFICACY; DRUG INHIBITION; HUMAN; INTRACRANIAL PRESSURE; NEUROGENIC INFLAMMATION; NONHUMAN; REVIEW;

ANIMALS; BRAIN EDEMA; BRAIN ISCHEMIA; CEREBROVASCULAR ACCIDENT; ENCEPHALITIS; HUMANS; SUBSTANCE P;

EID: 34547793705     PISSN: 02140934     EISSN: None     Source Type: Journal    
DOI: 10.1358/dnp.2007.20.4.1103527     Document Type: Review

References (59)

1. Bakhai, A. The burden of coronary, cerebrovascular and peripheral arterial disease. Pharmacoeconomics 2004, 22 (Suppl. 4): 11-8.
2. Dewey, H.M., Thrift, A.G., Mihalopoulos, C. et al. Cost of stroke in Australia from a societal perspective: Results from the North East Melbourne Stroke Incidence Study (NEMESIS). Stroke 2001, 32: 2409-16.
3. Rosenberg, G.A. Ischemic brain edema. Prog Cardiovasc Dis 1999, 42: 209-16.
4. Heuschmann, P.U., Berger, K., Misselwitz, B. et al. Frequency of thrombolytic therapy in patients with acute ischemic stroke and the risk of in-hospital mortality: The German Stroke Registers Study Group. Stroke 2003, 34: 1106-13.
5. Katzan, I.L., Furlan, A.J., Lloyd, L.E. et al. Use of tissue-type plasminogen activator for acute ischemic stroke: The Cleveland area experience. JAMA 2000, 283: 1151-8.
6. Hill, M.D. and Hachinski, V. Stroke treatment: Time is brain. Lancet 1998, 352 (Suppl. 3): SIII10-14.
7. Lipton, P. Ischemic cell death in brain neurons. Physiol Rev 1999, 79: 1431-568.
8. Dirnagl, U., Iadecola, C. and Moskowitz, M.A. Pathobiology of ischemic stroke: an integrated view. Trends Neurosci 1999, 22: 391-7.
9. Hacke, W., Schwab, S., Horn, M. et al. 'Malignant' middle cerebral artery territory infarction: Clinical course and prognostic signs. Arch Neurol 1996, 53: 309-15.
10. Bath, P.M.W. Optimising homeostasis. Br Med Bull 2000, 56: 422-35.
11. Green, A.R. Why do neuroprotective drugs that are so promising in animals fail in the clinic? An industry perspective. Clin Exp Pharmacol Physiol 2002, 29: 1030-4.
12. Gartshore, G., Patterson, J. and Macrae, I.M. Influence of ischemia and reperfusion on the course of brain tissue swelling and blood-brain barrier permeability in a rodent model of transient focal cerebral ischemia. Exp Neurol 1997, 147: 353-60.
13. Ayata, C. and Ropper, A.H. Ischemic brain edema. J Clin Neurosci 2002, 9: 113-24.
14. Betz, A.L. and Coester, H.C. Effect of steroid therapy on ischemic brain edema and blood to brain sodium transport. Acta Neurochir Suppl (Wien) 1990, 51: 256-8.
15. Betz, A.L. and Coester, H.C. Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats. Stroke 1990, 21: 1199-204.
16. Morris, J.W. and Hachinski, V.C. High dose steroid treatment in cerebral infarction. Br Med J (Clin Res Ed) 1986, 292: 21-3.
17. Woodcock, J., Ropper, A.H. and Kennedy, S.K. High dose barbiturates in non-traumatic brain swelling: ICP reduction and effect on outcome. Stroke 1982, 13: 785-7.
18. Schwab, S., Spranger, M., Schwarz, S. et al. Barbiturate coma in severe hemispheric stroke: useful or obsolete? Neurology 1997, 48: 1608-13.
19. Yatsu, F.M., Diamond, I., Graziano, C. et al. Experimental brain ischemia: Protection from irreversible damage with a rapid-acting barbiturate (methohexital). Stroke 1972, 3: 726-32.
20. Chen, H.J., Lee, T.C. and Wei, C.P. Treatment of cerebellar infarction by decompressive suboccipital craniectomy. Stroke 1992, 23: 957-61.
21. Lanzino, D.J. and Lanzino, G. Decompressive craniectomy for space-occupying supratentorial infarction: Rationale, indications, and outcome. Neurosurg Focus 2000, 8: e3.
22. Klatzo, I. Pathophysiological aspects of brain edema. Acta Neuropathol (Berl) 1987, 72: 236-9.
23. Menzies, S.A, Betz, A.L. and Hoff, J.T. Contributions of ions and albumin to the formation and resolution of ischemic brain edema. J Neurosurg 1993, 78: 257-66.
24. Quast, M.J., Huang, N.C., Hillman, G.R. et al. The evolution of acute stroke recorded by multimodal magnetic resonance imaging. Magn Reson Imaging 1993, 11: 465-71.
25. Woie, K., Koller, M.E., Heyeraas, K.J. et al. Neurogenic inflammation in rat trachea is accompanied by increased negativity of interstitial fluid pressure. Circ Res 1993, 73: 839-45.
26. Bayliss, W.M. On the origin from the spinal cord of the vaso-dilator fibers of the hindlimb, and on the nature of these fibers. J Physiol 28 1901; 26: 173-209.
27. Black, P.H. Stress and the inflammatory response: A review of neurogenic inflammation. Brain Behav Immun 2002, 16: 622-53.
28. Severini, C., Improta, G., Falconieri-Erspamer, G. et al. The tachykinin peptide family. Pharmacol Rev 2002, 54: 285-322.
29. Kuroiwa, T., Cahn, R., Juhler, M. et al. Role of extracellular proteins in the dynamics of vasogenic brain edema. Acta Neuropathol (Berl) 1985, 66:3-11.
30. Kuroiwa, T., Ting, P., Martinez, H. et al. The biphasic opening of the blood-brain barrier to proteins following temporary middle cerebral artery occlusion. Acta Neuropathol (Berl) 1985, 68: 122-9.
31. Holzer, P. Neurogenic vasodilatation and plasma leakage in the skin. Gen Pharmacol 1998, 30: 5-11.
32. Otsuka, M. and Yoshioka, K. Neurotransmitter functions of mammalian tachykinins. Physiol Rev 1993, 73: 229-308.
33. Gadduni, J.H. and Schild, H. Depressor substances in extracts of intestine. J Physiol 1934, 83: 1-14.
34. Campos, M.M. and Calixto, J.B. Neurokinin mediation of edema and inflammation. Neuropeptides 2000, 34: 314-22.
35. Matsas, R., Kenny, A.J. and Turner, A.J. The metabolism of neuropeptides. The hydrolysis of peptides, including enkephalins, tachykinins and their analogues, by endopeptidase-24.11. Biochem J 1984, 223: 433-40.
36. Skidgel, R.A. and Erdos, E.G The broad substrate specificity of human angiotensin I converting enzyme. Clin Exp Hypertens A. 1987, 9: 243-59.
37. Alves, R.V., Campos, M.M., Santos, A.R. et al. Receptor subtypes involved in tachykinin-mediated edema formation. Peptides 1999, 20: 921-7.
38. Ribeiro-da-Silva, A. and Hokfelt, T. Neuroanatomical localisation of Substance P in the CNS and sensory neurons. Neuropeptides 2000, 34: 256-71.
39. Cao, T., Gerard, N.P. and Brain, S.D. Use of NK(1) knockout mice to analyze substance P-induced edema formation. Am J Physiol 1999, 277 (2Pt. 2): R476-81.
40. Harrison, S. and Geppetti, P. Substance p. Int J Biochem Cell Biol 2001, 33: 555-76.
41. Rupniak, N.M., Carlson, B.C., Harrison, T. et al. Pharmacological blockade or genetic deletion of substance P (NK(1)) receptors attenuates neonatal vocalisation in guineapigs and mice. Neuropharmacol 2000, 39: 1413-21.
42. Hokfelt, T., Zhang, X. and Wiesenfeld-Hallin, Z. Messenger plasticity in primary sensory neurons following axotomy and its functional implications. Trends Neurosci 1994, 17: 22-30.
43. Noguchi, K., Morita, Y., Kiyama, H. et al. A noxious stimulus induces the preprotachykinin-A gene expression in the rat dorsal root ganglion: A quantitative study using in situ hybridization histochemistry. Brain Res 1988, 464: 31-5.
44. McCarson, K.E. Central and peripheral expression of neurokinin-1 and neurokinin-3 receptor and substance P-encoding messenger RNAs: Peripheral regulation during formalin-induced inflammation and lack of neurokinin receptor expression in primary afferent sensory neurons. Neurosci 1999, 93: 361-70.
45. Stumm, R., Culmsee, C., Schafer, M.K. et al. Adaptive plasticity in tachykinin and tachykinin receptor expression after focal cerebral ischemia is differentially linked to gabaergic and glutamalergic cerebrocortical circuits and cerebrovenular endothelium. J Neurosci 2001, 21: 798-811.
46. Nimmo, A.J., Cernak, I., Heath, D.L. et al. Neurogenic inflammation is associated with development of edema and functional deficits following traumatic brain injury in rats. Neuropeptides 2004, 38: 40-7.
47. Vink, R., Young, A., Bennett, C.J. et al. Neuropeptide release influences brain edema formation after diffuse traumatic brain injury. Acta Neurochir Suppl 2003, 86: 257-60.
48. Yu, Z., Cheng, G., Huang, X. et al. Neurokinin-1 receptor antagonist SR140333: A novel type of drug to treat cerebral ischemia. Neuroreport 1997, 8: 2117-9.
49. Bruno, G., Tega, F., Bruno, A. et al. The role of substance P in cerebral ischemia. Int J Immunopathol Pharmacol 2003, 16: 67-72.
50. Turner, R.J., Blumbergs, P.C., Sims, N.R. et al. Increased substance P immunoreactivity and edema formation following reversible ischemic stroke. Acta Neurochir Suppl 2006, 96: 263-6.
51. Vink, R. and Nimmo, A.J. Novel therapies in development for the treatment of traumatic brain injury. Expert Opin Investig Drugs 2002, 11: 1375-86.
52. Malcangio, M., Ramer, M.S., Jones, M.G. et al. Abnormal substance P release from the spinal cord following injury to primary sensory neurons. Eur J Neurosci 2000, 12: 397-9.
53. Sharma, H.S., Nyberg, F., Olsson, Y. et al. Alteration of substance P after trauma to the spinal cord: An experimental study in the rat. Neuroscience 1990, 38: 205-12.
54. Persson, M.G., Hedqvist, P. and Gustafsson, L.E. Nerve-induced tachykinin-mediated vasodilation in skeletal muscle is dependent on nitric oxide formation. Eur J Pharmacol 1991, 205: 295-301.
55. Gauchy, C., Desban, M., Glowinski, J. et al. Distinct regulations by septide and the neurokinin-1 tachykinin receptor agonist [pro9]substance P of the N-methyl-D-aspartate-evoked release of dopamine in striosome- and matrix-enriched areas of the rat striatum. Neuroscience 1996, 73: 929-39.
56. Anderson, J.J., Chase, T.N. and Engber, T.M. Substance P increases release of acetylcholine in the dorsal striatum of freely moving rats. Brain Res 1993, 623: 189-94.
57. Shen, K.Z. and North, R.A. Substance P opens cation channels and closes potassium channels in rat locus coeruleus neurons. Neurosci 1992, 50: 345-53.
58. Parker, D., Zhang, W. and Grillner, S. Substance P modulates NMDA responses and causes long-term protein synthesis-dependent modulation of the lamprey locomotor network. J Neurosci 1998, 18: 4800-13.
59. Kramer, J.H., Phillips, T.M. and Weglicki, W.B. Magnesium-deficiency- enhanced post-ischemic myocardial injury is reduced by substance P receptor blockade. J Mol Cell Cardiol 1997, 29: 97-110.