Role of leukocytes in reperfusion injury of skeletal muscle after partial ischemia

J. Yokota, J. P. Minei, G. A. Fantini, G. T. Shires

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7 Scopus citations


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 languageEnglish (US)
Pages (from-to)26/4
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4
StatePublished - 1989

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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