Previous studies by others indicated that PGs were present in brain, spinal cord, and c.s.f. of several mammalian species. In the present study we compared levels of
PGE and
PGF by R.I.A. in spinal cord tissue from traumatized cats and cats pretreated with
indomethacin prior to
trauma to those of baseline and
sham operated controls in order to assess for the first time, to our knowledge, whether meaningful changes in levels of
PGE and
PGF could be detected which might shed new light on the etiology of
spinal cord trauma. Levels of
PGF (nanograms/gram wet wt) in the cord segment immediately adjacent to the point of
trauma were 8.05 +/- 1.50, and 13.13 +/- 1.38 for baseline and
sham operated cats respectively. Spinal
trauma led to more than a 100% increase in
PGF levels to 29.26 +/- 3.58. Although pretreatment with
indomethacin 30 min prior to
trauma gave the expected blockade of the
PGF response to
trauma, a measurable level of
PGF (2.55 +/- 0.17) was found in the cord after
indomethacin. Cord levels of
PGF declined after 3 hr in both
sham operated and traumatized animals.
PGF was maximally stimulated by
trauma during the first 3 hr with little effect at 72 hr. Although carefully examined,
PGE levels in cat spinal cord appeared to be virtually unaffected by
trauma. These findings clearly demonstrate for the first time that traumatic injury to the spinal cord is accompanied by marked increases in PG levels at the site of
trauma, and that the observed elevation in
PGF in response to
trauma can be blocked by
indomethacin in vivo. Whether
PGF changes are causally related to the etiology of
spinal cord trauma, or merely represent a manifestation of PG release as a result of non-specific tissue injury, remains to be seen.