Neutrophils have been implicated as mediators of the reperfusion injury following ischemia. In order to measure neutrophil activation, O2- was determined after 2 hr of ischemia followed by 1 hr of reperfusion (no clinical reperfusion injury) and 3 hr of ischemia followed by 1 hr of reperfusion (significant clinical reperfusion injury). Using New Zealand white rabbits, baseline blood samples were drawn from an ear artery. The right iliac and femoral arteries were exposed and clamped. Just prior to clamp release, blood was obtained from the right iliac vein (ischemia). After 1 hr of reperfusion, blood was again taken from the right iliac vein (reperfusion). Neutrophils were isolated from the blood samples. O2- was determined by the reduction of cytochrome e using a spectrophotometer. In the 2-hr group, results (expressed as μmole O2-/min/2 × 106 cells) were: baseline, 0.337 ± 0.025; ischemia, 0.512 ± 0.039;* and reperfusion, 0.634 ± 0.064*. (*P < .05 as compared to baseline). In the 3-hr group, results were: baseline, 0.391 ± 0.038; ischemia, 0.413 ± 0.051; and reperfusion, 0.258 ± 0.043** (**P < 0.05 as compared to 2 hr reperfusion). A significant increase in O2- was seen after 2 hr of ischemia followed by 1 hr of reperfusion. However, little O2- increase was seen after 3 hr of ischemia and a significant O2- decrease was seen after 1 hr of reperfusion. We conclude: (1) Neutrophil O2 is stimulated early in ischemia followed by reperfusion; (2) after reperfusion injury occurs (3 hr), neutrophils have been activated and O2- can no longer be stimulated; and (3) O2- in this model may be involved in the clinical reperfusion injury seen.
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