Microvascular basal lamina antigen loss after traumatic brain injury in the rat

The loss of microvascular basal lamina antigen is known to be a consequence of cerebral ischemia, but little information is available on its role in traumatic brain injury (TBI). The aim of our study was (1) to test the hypothesis that there is damage to the basal lamina of brain microvasculature after TBI, (2) to localize microvascular damage, and (3) to compare this loss with that in ischemia. Rats (n=14) were either sham operated (n=5) or subjected to fluid percussion injury (n=9; TBI=1.5 atm) and killed after 0 (n=5, sham), 12 (n=4), or 24 h (n=5). Collagen-type-IV immunoreactivity and a digital image-processing system were used to localize and quantify the number of stained vascular elements and the total collagen stained area. Western blot was used to compare collagen-type-IV content on the traumatic and nontraumatic brain side. The cortex of animals subjected to TBI and killed after 24 h showed a reduction in the area of stained collagen amounting to 19+/-4% (p<0.009) and a reduction in the total number of microvessels identified by collagen stain (29+/-6%; p<0.02). The Western blot revealed a 31+/-6% (p<0.03) reduction of collagen, compared to the mirror cortical area after 24 h. No significant reduction was found in the group that survived 12 h or in basal ganglia in both groups. TBI causes microvascular basal lamina damage. Whereas TBI affected only cortical areas, cerebral ischemia also induced microvascular basal lamina damage in the basal ganglia. After 24 h, the extent of severe basal lamina damage due to TBI was less severe than in ischemia.