Korean J Physiol Pharmacol.
2000 Dec;4(6):525-530.
The effect of indomethacin on the production of eicosanoids and edema
during ischemia-reperfusion injury in skeletal muscle
- Affiliations
-
- 1Department of Pharmacology, College of Medicine, Dankook University,
San 29 Anseodong, Cheonan, Choongnam, South Korea.
hgkimm@anseo.dankook.ac.kr
Abstract
- During reperfusion of skeletal muscle after ischemia, lipid mediators,
mainly eicosanoids, are released and may have a role in the
pathogenesis of reperfusion injury. To validate the role of eicosanoids
in the ischemia-reperfusion induced functional deficits in skeletal
muscle, we compared muscle edema and the changes of eicosanoid
concentration in the rat hind limb after ischemia-reperfusion injury by
application of tourniquet. After 4 hours of ischemia, reperfusion was
established for 4 hours by releasing tourniquet. To assess tissue
damage, edema, and wet/dry weight ratios were determined and the
eicosanoid concnentrations were measured by the HPLC. The muscle edema
and the release of cyclooxygenase metabolites were not induced by the
ischemia itself rather they were significantly increased by
reperfusion. Indomethacin treatment ameliorated limb edema and
decreased the release of 6-keto-PGF1alpha, thromboxane B2, and PGE2
induced by reperfusion. But the inhibitory effect of indomethacin on
edema (35%) was relatively low than the inhibitory effect on release of
cyclooxygenase metabolites (up to 69%) by reperfusion. These results
support the view that cyclooxygenase products may play a significant
role in the formation of muscle injury by ischemia-reperfusion and
suggest that nonsteroidal antiinflammatory agents might be partially
beneficial to the management of acute limb ischemia-reperfusion injury.