OBJECTIVE: The primary objective of this study was to investigate the
potential contribution of vasospasm to the cascade of secondary injury
processes after traumatic spinal cord injury. Although ischemic facto
rs have been implicated, in that vessel rupture, compression, and intr
avascular thrombosis are readily identifiable, vasospasm has been more
difficult to detect. METHODS: The sulcal arterioles in the ventral me
dian fissure of the cervical spinal cord from adult rats were quantita
tively examined at the ultrastructural level up to 24 hours after comp
ression injury. RESULTS: There were statistically significant changes
in the luminal cross-sectional area of sulcal arterioles after spinal
cord injury, correlating directly with decreases in length and increas
es in width of medial smooth muscle cells. A simple mathematical model
of postinjury blood flow is presented, suggesting an 80% decrease cau
sed by vasospasm alone. CONCLUSION: Our results clearly implicate vaso
spasm as a contributing factor to secondary injury processes after tra
umatic spinal cord injury.