Prostaglandins modulate alterations of microvascular permeability, blood flow, edema and serotonin levels following spinal cord injury: an experimental study in the rat.

The possibility that prostaglandins influence edema formation, microvascular permeability increase and reduction of blood flow following spinal cord trauma was examined in a rat model. In addition, the influence of prostaglandins on serotonin metabolism of the traumatized spinal cord was evaluated. Trauma to spinal cord (2-mm-deep and 5-mm-long incision in the right dorsal horn of T10-11 segments) resulted in a profound increase of the water content 5 h after injury. At this time, the microvascular permeability to Evans Blue and [131I]sodium was increased by 457 and 394%, respectively. The blood flow was reduced by 30%. The serotonin (5-hydroxytryptamine) content of the spinal cord increased by 205%. The plasma serotonin level rose by 152% in the injured group of rats. Pretreatment with indomethacin (10 mg/kg, i.p.) 30 min before trauma significantly reduced the edema and microvascular permeability increase. The local spinal cord blood flow of traumatized animals was partially restored. The increases of serotonin levels of the spinal cord and plasma were significantly attenuated. These beneficial effects of indomethacin were not present in rats given a lower dose (5 mg/kg). Indomethacin in either dose did not influence these parameters of control rats without trauma to the cord. Since indomethacin is a potential inhibitor of prostaglandins synthesis our observations indicate: (i) that prostaglandins participate in many microvascular responses (permeability changes, edema, blood flow) occurring after a trauma to the spinal cord; (ii) that these effects of the drug seem to be dose dependent, and (iii) that the prostaglandins may influence the serotonin metabolism following trauma to the spinal cord.