SUPPRESSION OF REPERFUSION INJURY IN RAT SKELETAL-MUSCLE BY ANTIOXIDATIVE ENZYMES

Citation
A. Yamamoto et al., SUPPRESSION OF REPERFUSION INJURY IN RAT SKELETAL-MUSCLE BY ANTIOXIDATIVE ENZYMES, Journal of clinical biochemistry and nutrition, 23(1), 1997, pp. 53-67
Citations number
27
ISSN journal
09120009
Volume
23
Issue
1
Year of publication
1997
Pages
53 - 67
Database
ISI
SICI code
0912-0009(1997)23:1<53:SORIIR>2.0.ZU;2-Y
Abstract
Prolonged skeletal muscle ischemia has been reported in acute arterial occlusion and crush syndrome. It often induces progressive edema and necrosis and occasionally life-threatening systemic complications, suc h as hypotension, hyperkalemia, acidosis, pulmonary edema, and acute r enal failure. As in other organs, ischemic injury in skeletal muscle i s initiated during hypoxia and is aggravated by reoxygenation during b lood reperfusion. This study aimed at examining the protective effect of antioxidative enzymes, superoxide dismutase and catalase, on ischem ia-reperfusion injury in skeletal muscle. Skeletal muscles in rat hind limb were subjected to in vivo ischemia by clamping both the infrarena l aorta and the bilateral femoral arteries for 4 h and to the subseque nt blood reperfusion for 1 h under profound anesthesia with pentobarbi tone. An attempt was made to suppress the muscle injury by infusing su peroxide dismutase and catalase 5 min before starting reperfusion. Tis sue water content was significantly increased by reperfusion. The incr ease in the water content was suppressed by the addition of those scav engers. Plasma levels of creatine phosphokinase and lactate dehydrogen ase were increased by ischemia and reperfusion. Addition of the scaven gers did not suppress these increases, indicating that scavengers were not effective in suppressing the cellular injury, which might have be gun during the ischemia and which might have been exacerbated by the r eperfusion. Mitochondrial oxidative phosphorylation was significantly suppressed by ischemia and reperfusion. Such scavengers restored the i nhibited mitochondrial function. These results indicate that the radic al scavengers tested were effective to protect mitochondrial functions against ischemia-reperfusion insults. Although the present study was carried out on an animal model, administration of these radical scaven gers may be effective to reduce injury due to acute arterial occlusion and crush syndrome.