EXPRESSION OF ENDOTHELIAL BARRIER ANTIGEN IMMUNOREACTIVITY IN BLOOD-VESSELS FOLLOWING COMPRESSION TRAUMA TO RAT SPINAL-CORD - TEMPORAL EVOLUTION AND RELATION TO THE DEGREE OF THE IMPACT

The endothelial barrier antigen (EBA) recognised by a monoclonal antib ody is expressed in rat cerebral microvessels possessing blood-brain b arrier properties but only weakly by fenestrated vessels. We have stud ied the expression of this marker in the spinal cord of control rats a nd compared the findings with those seen in rats subjected to compress ion injury at the T8-9 level with a survival period of 4 h, 24 h, 4 da ys and 9 days. To that end, formalin-fixed paraffin-embedded material was immunostained by the avidin-biotin-peroxidase complex method. Sect ions from control rats presented a distinct immunostaining at the site of the endothelial cells of almost all microvessels in the grey and w hite matter of the cord. The anterior and posterior spinal arteries di d not show such staining. Neurons and glial cells were unstained. Rats which had survived 4 h after a moderate or severe compression trauma still showed immunoreactivity in intramedullary microvessels at the si te of injury. There was a moderate reduction of vascular immunoreactiv ity at 24 h and a pronounced loss of such reactivity at 4 days after t rauma. At 9 days after compression the expression of the endothelial b arrier antigen had almost been normalised in the microvessels of the c ord. In conclusion, using immunohistochemistry, EBA can be demonstrate d in noninjured rat spinal cord microvessels, while the staining disap pears at the site of compression trauma to the cord. The EBA marker ca n be used to indicate sites of vascular injury in spinal cord compress ion injury. The factors causing the disappearance and restitution of t he antigen are unknown.