Trauma-induced opening of the the blood-spinal cord barrier is reduced by indomethacin, an inhibitor of prostaglandin biosynthesis. Experimental observations in the rat using [131I]-sodium, Evans blue and lanthanum as tracers
Affiliations: Laboratory of Neuropathology, University Hospital, S-751 85 Uppsala, Sweden | Department of Pharmaceutical Biosciences, Biomedical Centre, Uppsala University, Uppsala, Sweden
Abstract: The possibility that prostaglandins participate in opening of the blood-spinal cord barrier (BSCB) after trauma was investigated by comparing rats given indomethacin (an inhibitor of prostaglandin synthesis) before trauma with untreated animals. The trauma was produced by making an incision into the right dorsal horn of the T10–11 segment. The BSCB was examined after 5 h using Evans blue, [131I]-sodium and lanthanum as tracers. A focal trauma to the cord resulted in widespread opening of the BSCB to [l3lI]-sodium in the C5 to L5 segments of the untreated rats. Evans blue extravasation was limited to the T9–T12 segments. Electron microscopy of microvessels in the T9 and T12 segments showed lanthanum diffusely in some endothelial cells, in vesicular profiles and basal lamina. On the other hand, indomethacin pretreatment prevented the extravasation of [131I]-sodium in segments located far away from the trauma. In segments closer to the trauma, the extravasation of radiotracer was markedly reduced. Extravasation of Evans blue was less pronounced. Spread of lanthanum into the basal lamina of microvessels was not present. The diffuse passage into the capillary endothelium was reduced and the incidence of cytoplasmic vesicles loaded with lanthanum was lower. Our results for the first time provide direct morphological evidence that prostaglandins are involved in the early, widespread opening of the BSCB after trauma to the cord.
