Abstract
Two sets of experiments were conducted to investigate whether oxygen-de rived free radicals are involved in the mechanism of ischemia/reperfusion (I/R) injury of skeletal muscle and vitamin E is effective in alleviating the injury.
In the first set of experiments, twenty adult mongrel dogs were divided into three groups: group 1 (n=7) control, group 2 (n = 6) I/R, and group 3 (n=7) I/R with 500 mg of vitamin E. Serum creatine phosphokinase (CPK) and lipid per oxides (LPO) were measured as markers of rhabdomyolysis and biomembrane injury due to oxygen-derived free radicals, respectively. CPK increased signifi cantly after reperfusion with a peak value of 38,000 ± 9,800 mU/mL in group 2, when compared with a peak value of 1,060 ± 290 mU/mL in group 3 (p < 0.02). LPO also significantly increased with a peak value of 20.4 ±3.7 nmol/mL in group 2, when compared with a peak value of 9.2 ± 2.2 nmol/mL in group 3 (p < 0.04).
In the second sets of experiments, 13 dogs were divided into two groups: group A (n=5) control and group B (n=8) I/R. Tissue LPO was measured eighteen hours after reperfusion in the gracilis muscle and gastrocnemius mus cle. The mean value of LPO in the gracilis muscle was 0.94 ± 0.46 nmol/mg protein in group A, compared with 1.13 ± 0.67 nmol/mg protein in group B. It was higher in group B, but there was no significant difference. Mean LPO in the gastrocnemius muscle was 0.85 ± 0.34 nmol/mg protein in group A, and 1.83 ± 0.71 nmol/mg protein in group B. There was a significant difference (p < 0.02).
Serum CPK and LPO were significantly higher in group 2 than in groups 1 and 3, and tissue LPO was also high in skeletal muscle after reperfusion. Serum CPK and LPO were effectively suppressed by administration of vitamin E be fore reperfusion.
These results show that oxygen-derived free radicals are involved in the mechanism of I/R injury in skeletal muscle and suggest that vitamin E is effec tive in alleviating the injury.
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