Abstract
It is well established that the spinal cord is subjected to inflammatory reactions in response to traumatic injury. Several investigators found a major reduction of blood flow in the spinal cord after injury, and vasospasm and thrombosis are considered as major causes of the ischemic insult’. Inflammatory responses underlying the secondary processes are initiated and regulated by specific signaling molecules. Among them vasoactive arachidonate metabolites (eicosanoids) play an important role; proaggregatory and vasoconstrictive thromboxane (TX) A2 as well as antiaggregatory and vasodilating prostaglandin (PG) I22. Cyclooxygenase isozymes (COX-1 and COX-2) are key enzymes, and proinflammatory cytokines like tumor necrosis factor (TNF)-a and interleukin (IL)-1 stimulate the eicosanoid synthesis by the induction of COX-2 in various cell types3,4. Recently, COX-2 induction in the central nervous system was demonstrated in response to seizures5and excitotoxin injection.
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