Segmental vascular resistance after mild controlled cortical impact injury in the rat.
In an effort to localize the site at which increased resistance occurs after brain trauma, pial arteriole diameter and pressure were assessed after mild controlled cortical impact (CCI) injury in rats using an open cranial window technique. The authors tested the hypothesis that an increase in resistance accompanied by vasoconstriction occurs at the level of the pial arterioles within the injured cortex of the brain. At 1 hour after mild CCI injury, ipsilateral cerebral blood flow was significantly reduced by 42% compared with sham injury (n = 4; < 0.05). Pial arteriole diameter and pressure remained unchanged. Resistance in the larger arteries (proximal resistance), however, was significantly greater after CCI injury (1.87 +/- 0.26 mm Hg/[mL. 100 g. min]) compared with sham injury (0.91 +/- 0.21 mm Hg/[mL. 100 g. min]; < 0.0001). Resistance in small vessels, arterioles, and venules (distal resistance) was also significantly greater after CCI injury (1.13 +/- 0.05 mm Hg/[mL. 100 g. min]) compared with sham injury (0.74 +/- 0.13 mm Hg/[mL. 100 g. min]; = 0.0001). The authors conclude that, at 1 hour after mild CCI injury, changes in vascular resistance comprise a 53% increase in the resistance distal to the area of injury and, surprisingly, a 105% increase in resistance in the arteries proximal to the injury site.
Golding
Elke M
EM
Department of Anesthesiology, Baylor College of Medicine, Houston, Texas 77030, USA. egolding@bcm.tmc.edu
Robertson
Claudia S
CS
Fitch
Jane C K
JC
Goodman
J Clay
JC
Bryan
Robert M
RM
D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure; D002196:Capillaries / Q000503:physiopathology; D002540:Cerebral Cortex / Q000293:injuries*; D002560:Cerebrovascular Circulation; D008297:Male; D010841:Pia Mater / Q000098:blood supply; D051381:Rats; D020318:Rats, Long-Evans; D012720:Severity of Illness Index; D014655:Vascular Resistance; D014949:Wounds, Nonpenetrating / Q000473:pathology / Q000503:physiopathology*