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Superoxide anion production by leukocytes exposed to post-ischemic skeletal muscle
J J Hernández-Maldonado1, E Teehan, C D Franco
1Department of Surgery, UMDNJ-New Jersey Medical School, Newark.
Abstract:
Superoxide anion (O2-) and polymorphonuclear leukocytes (PMNs) have been implicated in the genesis of skeletal muscle ischemia-reperfusion (I-R) injury, but the source of (O2-) has not been established. We studied PMNs as a potential source of O2- using a ferricytochrome reduction assay in 5 anesthetized dogs. Using a gracilis muscle model of I-R, 6 hours of ischemia was followed by 2 hours of reperfusion. The contralateral muscle served as control. Prior to ischemia and after 0.5 and 2.0 hours of reperfusion, PMNs were separated from the gracilis venous effluent of ischemic (I) and control (C) muscles. Central venous samples were also obtained prior to surgical preparation and after reperfusion. Assays for O2- were performed with and without zymosan (Z) activation. Results are expressed as nmol O2-/2 x 10(6) PMNs +/- SEM. Baseline production of O2- was 0.49 +/- 0.54 in central venous samples; Z increased the values to 6.77 +/- 2.13. After 2 hrs of reperfusion, central O2- was 1.57 +/- 0.75, which increased to 7.1 +/- 1.04 with Z. Gracilis venous samples O2- values with and without Z are reported in Table I. One way measures of analysis of variance showed no significant (p > 0.05) differences between samples. Our results demonstrate that PMNs are not the sole source of O2- in the pathophysiology of skeletal muscle I-R injury. PMN associated injury may be mediated by mechanisms other than O2- production.
Insights
Polymorphonuclear leukocytes (PMNs) do not appear to be the sole source of superoxide anion (O2-) in skeletal muscle ischemia-reperfusion (I-R) injury. This suggests PMN-related injury may involve mechanisms beyond O2- production.
Area of Science:
- Biomedical Science
- Physiology
- Surgical Research
Background:
- Skeletal muscle ischemia-reperfusion (I-R) injury is a significant clinical concern.
- Superoxide anion (O2-) and polymorphonuclear leukocytes (PMNs) are implicated in I-R injury pathogenesis.
- The specific source of O2- in skeletal muscle I-R injury remains unclear.
Purpose of the Study:
- To investigate polymorphonuclear leukocytes (PMNs) as a potential source of superoxide anion (O2-) in skeletal muscle ischemia-reperfusion (I-R) injury.
- To determine if PMN-derived O2- contributes significantly to the pathophysiology of I-R injury.
Main Methods:
- Utilized a canine gracilis muscle model of I-R.
- Collected venous effluent from ischemic and control muscles, along with central venous samples.
- Measured O2- production in PMNs using a ferricytochrome reduction assay, with and without zymosan activation.
Main Results:
- No significant differences in O2- production were observed between PMNs from ischemic and control muscles.
- PMNs did not demonstrate a significant increase in O2- production post-reperfusion.
- Baseline and post-reperfusion O2- production in central venous samples showed variability but did not implicate PMNs as the sole source.
Conclusions:
- Polymorphonuclear leukocytes (PMNs) are not the sole source of superoxide anion (O2-) in skeletal muscle ischemia-reperfusion (I-R) injury.
- The contribution of PMNs to I-R injury may be mediated by pathways independent of O2- production.
- Further research is needed to elucidate the precise mechanisms of PMN involvement in I-R injury.