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Type: Book chapter
Title: Substance P antagonists as a novel intervention for brain edema and raised intracranial pressure
Author: Gabrielian, L.
Helps, S.
Thornton, E.
Turner, R.
Leonard, A.
Vink, R.
Citation: Brain Edema XV, 2013 / Katayama, Y., Maeda, T., Kuroiwa, T. (ed./s), vol.118, pp.201-204
Publisher: Springer
Publisher Place: Vienna
Issue Date: 2013
Series/Report no.: Acta Neurochirurgica Supplement; 118
ISBN: 9783709114346
Editor: Katayama, Y.
Maeda, T.
Kuroiwa, T.
Statement of
Levon Gabrielian, Stephen C. Helps, Emma Thornton, Renée J. Turner, Anna V. Leonard, and Robert Vink
Abstract: Increased intracranial pressure (ICP) following acute brain injury requires the accumulation of additional water in the intracranial vault. One source of such water is the vasculature, although the mechanisms associated with control of blood–brain barrier permeability are unclear. We have recently shown that acute brain injury, such as neurotrauma and stroke, results in perivascular accumulation of the neuropeptide, substance P. This accumulation is associated with increased blood–brain barrier permeability and formation of vasogenic edema. Administration of a substance P antagonist targeting the tachykinin NK1 receptor profoundly reduced the increased blood–brain barrier permeability and edema formation, and in small animal models of acute brain injury, improved functional outcome. In a large, ovine model of experimental traumatic brain injury, trauma resulted in a significant increase in ICP. Administration of an NK1 antagonist caused a profound reduction in post-­traumatic ICP, with levels returning to normal within 4 h of drug administration. Substance P NK1 antagonists offer a novel therapeutic approach to the treatment of acute brain injury.
Keywords: Neurotrauma
Neuro­­genic inflammation
Description: Proceedings: The XVth International Symposium of Brain Edema and Cellular Injury, Tokyo, 22–24 October 2011
Rights: © Springer-Verlag Wien 2013
DOI: 10.1007/978-3-7091-1434-6_37
Appears in Collections:Anatomical Sciences publications
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