Jj. Hernandezmaldonado et al., SUPEROXIDE ANION PRODUCTION BY LEUKOCYTES EXPOSED TO POSTISCHEMIC SKELETAL-MUSCLE, Journal of Cardiovascular Surgery, 33(6), 1992, pp. 695-699
Superoxide anion (O2-) and polvmorphonuclear leukocytes (PMNs) have be
en implicated in the genesis of skeletal muscle ischemia-reperfusion (
I-R) injury, but the source of (O2-) has not been established. We stud
ied PMNs as a potential source of O2- using a ferricytochrome reductio
n 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 contra
lateral 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 samp
les were also obtained prior to surgical preparation and after reperfu
sion. Assays for O2- were performed with and without zymosan (Z) activ
ation. Results are expressed as nmol O2-/2 x 10(6) PMNs +/- SEM. Basel
ine production of O2- was 0.49 +/- 0.54 in central venous samples; Z i
ncreased the values to 6.77 +/- 2.13. After 2 hrs of reperfusion, cent
ral O2- was 1.57 +/- 0.75, which increased to 7.1 +/- 1.04 with Z. Gra
cilis venous samples O2- values with and without Z are reported in Tab
le I. One way measures of analysis of variance showed no significant (
p > 0.05) differences between samples. Our results demonstrate that PM
Ns are not the sole source of O2- in the pathophysiology of skeletal m
uscle I-R injury. PMN associated injury may be mediated by mechanisms
other than O2- production.