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Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia 22908
The
relative contribution of xanthine oxidase (XO) and leukocytes to tissue
injury after short-term ischemia is unknown. In this study, we
subjected three groups of rat spinotrapezius muscles to 30-min
ischemia and 1-h reperfusion: 1)
ischemia-reperfusion (I/R) + 0.9% saline, 2) I/R + superoxide dismutase, and 3) I/R + oxypurinol. A
fourth group served as nonischemic control. We quantified
the increase in resistance (%
R) caused by
leukocyte-capillary plugging concurrently with myocyte uptake of
propidium iodide (PI) [expressed as no. of PI spots per total
volume of perfused tissue (NPI/V)] and
performed assays to quantify XO activity, thiobarbituric acid-reactive
substances (TBARS), and myeloperoxidase (MPO). Groups 2 and
3 exhibited significant decreases in NPI/V relative to group 1. MPO levels and TBARS were similar among
all groups, and mean %R was significantly reduced in
groups 2 and 3 relative to group 1. However,
elevated XO was observed in groups 1 and 2 relative to
group 3 and nonischemic controls. These data are consistent
with the hypothesis that XO, rather than toxic species produced by
plugging or venule-adherent leukocytes, is responsible for postischemic
damage in this model.
xanthine oxidase; superoxide dismutase; oxypurinol; white blood cells; microcirculation
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