EXPERIMENTAL NEOPLASTIC SPINAL-CORD COMPRESSION - EFFECT OF ANTIINFLAMMATORY AGENTS AND GLUTAMATE RECEPTOR ANTAGONISTS ON VASCULAR-PERMEABILITY

It has been demonstrated in paraplegic rats harboring an epidural neoplasm that an antiedema effect can be achieved by in vivo treatment with either steroidal or nonsteroidal anti-inflammatory agents or by glutamate receptor antagonists. The effect of these treatments on vascular permeability of the normal and compressed spinal cord was quantitiated by the Evans blud dye technique. Tumor-free and tumor-bearing rats were assigned randomly for treatment as follows: 0.5 ml of saline or three doses at 12-hour intervals ofeither dexamethasone (5 mg/kg), methylprednisolone (30 mg/kg), indomethacin (5 mg/kg every 24 hours), or a single dose of either ketamine (110 mg/kg) or MK-801 (3 mg/kg). Treatment was given at the onset of paraplegia, and the animals were killed after 30 hours. In tumor-bearing rats in the early symptomatic stage, extravasation of Evans blue dye was 4.8 times greater than that of the normal cord (P < 0.001) and at the onset of paraplegia it was 9.9 times greater (P < 0.0006). Glucocorticoids and indomethacin reduced dye extravasation in paraplegic animals (P < 0.01 and P < 0.003, respectively), but the decreased permeability induced by ketamine and MK-801 did not reach the level of significance. In tumor-free control animals permeability was not changed by administration of either glucocorticoids or indomethacin but was significantly reduced by ketamine or MK-801 (P < 0.01). It is suggested that the disparity in the effect on vascular permeability between the anti-inflammatory agents and glutamate receptor antagonists in the normal and the pathological states offers further support to the concept that spinal cord edema in epidural compression is probably related to both vasogenic and cytotoxic edema.