Stroke, Vol 13, 494-499, Copyright © 1982 by American Heart Association
E Shohami, J Rosenthal and S Lavy
Rats were subjected to severe incomplete cerebral ischemia followed by
recirculation. The levels of several of the cyclooxygenase products of
arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30
minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated
during the first 5 min. of ischemia and its level declined at 15 min. and
returned to control level at 30 min. of recirculation. TXB2, on the other
hand, increased during the whole time course of the experiment and at the
end of the post ischemic period its level was 5 times higher than control.
Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to
ischemia reduced the levels of these products without altering the pattern
of their changes. During the ischemic period the EEG was isoelectric and
the mean recovery time of electrical cortical activity after 15 min. of
ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received
indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to
the induction of ischemia. We suggest that the reversibility of cortical
activity may be correlated to the accumulation of TXB2 during ischemia and
recirculation, and inhibition of its synthesis might improve the post-
ischemic reflow.
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The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain
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