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Type: Book chapter
Title: The effect of an NK1 receptor antagonist on blood spinal cord barrier permeability following balloon compression-induced spinal cord injury
Author: Leonard, A.
Vink, R.
Citation: Brain Edema XV, 2013 / Katayama, Y., Maeda, T., Kuroiwa, T. (ed./s), pp.303-306
Publisher: Springer
Publisher Place: Vienna
Issue Date: 2013
Series/Report no.: Acta Neurochirurgica Supplement; 118
ISBN: 9783709114339
Statement of
Responsibility: 
Anna V. Leonard and Robert Vink
Abstract: The blood spinal cord barrier (BSCB) is disrupted following spinal cord injury (SCI) resulting in vasogenic edema and increased intrathecal pressure (ITP). The neuropeptide substance P (SP) has been implicated in the development of blood–brain barrier (BBB) disruption, edema, and increased intracranial pressure following brain injury, although it has not been investigated in SCI. The balloon compression model of experimental SCI has many advantages in that it replicates the “closed” environment observed clinically. Accordingly, this study characterized whether this model produces an increase in BSCB permeability and edema, and whether a SP, NK1 tachykinin receptor antagonist, N-acetyl-l-tryptophan (NAT) reduces such BSCB disruption and edema formation. At 30 min post-injury, animals were administered 2.5 mg/kg NAT or saline. Subgroups of animals were assessed for BSCB permeability (Evan’s Blue) and spinal cord edema (wet weight/dry weight). BSCB permeability and edema were significantly increased in injured groups compared with sham (p < 0.001). There was no significant difference between vehicle and NAT treatment. We conclude that the balloon compression model of SCI produces significant BSCB disruption although NAT treatment did not attenuate BSCB permeability or edema. Further studies are required to fully elucidate the role of SP following SCI.
Keywords: Spinal cord injury; Blood spinal cord barrier permeability; Edema; Substance P; Neurogenic inflammation
Description: Proceedings: The XVth International Symposium of Brain Edema and Cellular Injury, Tokyo, 22–24 October 2011
Rights: © Springer-Verlag Wien 2013
RMID: 0020131379
DOI: 10.1007/978-3-7091-1434-6_59
Appears in Collections:Anatomical Sciences publications

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