These experiments evaluated the leukocyte as a potential source of oxygen free radical (OFR) generation during reperfusion injury in post-ischemic skeletal muscle. The infrarenal aorta of heparinized Sprague-Dawley rats was clamped for 90 min, declamped, and reperfused for 60 min. Hindlimb muscle resting transmembrane potential difference (E(m)) and high-energy phosphate content were determined at base line, during ischemia, and on reperfusion. Four groups were studied: a control group, a second group receiving superoxide dismutase and catalase (SOD + CAT) on declamping, a third group receiving dimethylmyleran (DMM) 7 days before the experiment to obtain a selective leukopenia (white blood cells = 1,210 ± 144/mm3, neutrophils = 1.2%), and a fourth group pretreated with allopurinol (ALLO). During the ischemic period, resting E(m) was significantly depolarized (-78.6 ± 0.5 mV from -90.3 ± 0.3; P < 0.05) in the control group, whereas creatine phosphate (CP) was depleted and ATP maintained. Data collected during the ischemic phase of the three other groups were similar to the control group (P = NS). On reperfusion, persistent depolarization of resting E(m) was observed despite restoration of muscle CP content in the control and ALLO groups (-75.4 and -77.0 mV, respectively). In contrast, significant repolarization of resting E(m) was noted after reperfusion in the SOD + CAT and DMM groups (-86.5 and -88.6 mV, respectively). These data implicate leukocyte-generated OFR as mediators of reperfusion-associated cellular membrane injury in postischemic skeletal muscle.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)