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.