A bradykinin BK2 receptor antagonist HOE-140 attenuates blood-spinal cord barrier permeability following a focal trauma to the rat spinal cord. An experimental study using Evans blue, [131]I-sodium and lanthanum tracers.

The role of bradykinin in breakdown of the blood-spinal cord barrier (BSCB) permeability following a focal lesion to the cord was examined using a potent bradykinin BK2 receptor antagonist, HOE-140 in a rat model. Spinal cord injury was produced by an incision into the right dorsal horn of the T10-11 segment. In a separate group of rats HOE-140 (1 mg/kg) was administered intravenously 30 min before injury. A focal trauma to the cord markedly increased the extravasation of Evans blue and [131]I-sodium tracers in the cord at 5 h. Pretreatment with HOE-140 significantly attenuated the extravasation of these tracers in the spinal cord. At ultrastructural level, lanthanum was seen within the endothelial cell cytoplasm, in vesicular profiles as well as in the basal lamina in the untreated traumatised rats. In HOE-140 treated rats, the lanthanum was mainly confined within the lumen. These observations strongly suggest that bradykinin is involved in the breakdown of the BSCB permeability probably via bradykinin BK2 receptors, not reported earlier.