Ultrastructural evidence for arteriolar vasospasm after spinal cord trauma.
OBJECTIVE
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.


METHODS
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.


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 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.


CONCLUSIONS
Our results clearly implicate vasospasm as a contributing factor to secondary injury processes after traumatic spinal cord injury.
Anthes
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Canadian Paraplegic Association Spinal Cord Injury Research Laboratory, Playfair Neuroscience Unit, Toronto Hospital, University of Toronto, Ontario, Canada.
Theriault
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Tator
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CH
D000818:Animals; D001160:Arterioles / Q000473:pathology; D001783:Blood Flow Velocity / Q000502:physiology; D005260:Female; D007511:Ischemia / Q000473:pathology*; D002546:Ischemic Attack, Transient; D008854:Microscopy, Electron; D008955:Models, Cardiovascular; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000098:blood supply*; D013119:Spinal Cord Injuries / Q000473:pathology*; D014661:Vasoconstriction / Q000502:physiology*; D014699:Venules / Q000473:pathology