Ultrastructural evidence for arteriolar vasospasm after spinal cord trauma.

Abstract

The primary objective of this study was to investigate the potential contribution of vasospasm to the cascade of secondary injury process after traumatic spinal cord injury. Although ischemic factors have been implicated, in that vessel rupture, compression, and intravascular thrombosis are readily identifiable, vasospasm has been more difficult to detect. The sulcal arterioles in the ventral median fissure of the cervical spinal cord from adult rats were quantitatively examined at the ultrastructural level up to 24 hours after compression injury. 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 increases in width of medial smooth muscle cells. A simple mathematical model of postinjury blood flow is presented, suggesting an 80% decrease caused by vasospasm alone. Our results clearly implicate vasospasm as a contributing factor to secondary injury processes after traumatic spinal cord injury.