The role of PMN in the reperfusion injury after ischemia is unclear. It was the purpose of this study to determine if PMN functions of phagocytosis and chemotaxis were altered after a brief period of ischemia (2 hr) followed by reperfusion (1 hr) in a model where no significant reperfusion injury occurred. Baseline blood samples were drawn from an ear artery from New Zealand white rabbits for PMN and serum. The right iliac and femoral arteries were clamped for 2 hr. Just prior to clamp release, blood was harvested from the right iliac vein. After 1 hr of reperfusion, blood was again harvested from the right iliac vein. Phagocytosis was measured by the percentage ingestion of zymosan by PMN. The zymosan beads had been opsonized with baseline (b), ischemia (i), or reperfusion (r) serum. Chemotaxis was evaluated by the number of PMN migrating across a filter. Serum obtained from b, i, and r blood samples served as the chemoattractants. Results for phagocytosis demonstrated a significant increase in i and r PMN as compared to b PMN. Opsonization by b, i, or r serum did not enhance this effect (ANOVA, F = 4.477; P = 0.0266). Similar increases in chemotaxis were observed for i and r PMN which also were not enhanced by the chemoattractants of b, i, or r serum (ANOVA, F = 25.43; P < 0.001). We conclude that (1) rabbit PMN phagocytosis and chemotaxis were increased after both 2 hr of ischemia and 1 hr of reperfusion, (2) this effect was not augmented by i or r serum, and (3) rabbit PMN functions of phagocytosis and chemotaxis were stimulated in this model after a brief period of ischemia and after reperfusion before a clinical reperfusion injury took place.
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