PROSTAGLANDINS MODULATE ALTERATIONS OF MICROVASCULAR PERMEABILITY, BLOOD-FLOW, EDEMA AND SEROTONIN LEVELS FOLLOWING SPINAL-CORD INJURY - ANEXPERIMENTAL-STUDY IN THE RAT

The possibility that prostaglandins influence edema formation, microva scular permeability increase and reduction of blood flow following spi nal cord trauma was examined in a rat model. In addition, the influenc e of prostaglandins on serotonin metabolism of the traumatized spinal cord was evaluated. Trauma to spinal cord (2-mm-deep and 5-mm-long inc ision in the right dorsal horn of TI 0-11 segments) resulted in a prof ound increase of the water content 5h after injury. At this time, the microvascular permeability to Evans Blue and [I-131]sodium was increas ed by 457 and 394%, respectively. The blood flow was reduced by 30%. T he serotonin (5-hydroxytryptamine) content of the spinal cord increase d by 205%. The plasma serotonin level rose by 152% in the injured grou p of rats. Pretreatment with indomethacin (10 mg/kg, i.p.) 30 min befo re trauma significantly reduced the edema and microvascular permeabili ty increase. The local spinal cord blood flow of traumatized animals w as partially restored. The increases of serotonin levels of the spinal cord and plasma were significantly attenuated. These beneficial effec ts of indomethacin were not present in rats given a lower dose (5 mg/k g). Indomethacin in either dose did not influence these parameters of control rats without trauma to the cord. Since indomethacin is a poten tial inhibitor of prostaglandins synthesis our observations indicate: (i) that prostaglandins participate in many microvascular responses (p ermeability changes, edema, blood flow) occurring after a trauma to th e spinal cord; (ii) that these effects of the drug seem to be dose dep endent, and (iii) that the prostaglandins may influence the serotonin metabolism following trauma to the spinal cord.