Neutrophils have been implicated as mediators of the reperfusion injury which occurs in skeletal muscle after ischemia. The purpose of this study is to determine if PMN chemotaxis occur 24 hr after an ischemic injury followed by reperfusion. Rabbit hindlimbs were made ischemic by clamping the right iliac and femoral arteries for 2 or 3 hr after ligating all pelvic collaterals. The limb was then reperfused by removing the clamps. After 24 hr of reperfusion, blood samples were drawn from the carotid artery and right iliac vein. Serum and PMN were isolated from each blood sample. Chemotaxis, as determined by migration across a filter, was measured in each group. One-way analysis of variance demonstrated a significant increase in chemotaxis in PMN isolated from the venous effluent of hind limbs which had undergone 3 hr of ischemia and 24 hr of reperfusion. PMN isolated from the carotid artery of the same animals had significantly less chemotactic activity. There were no significant differences from control in PMN chemotaxis in specimens from sham animals or animals exposed to 2 hr of ischemia and 24 hr of reperfusion. Those rabbits which had undergone 3 hr of ischemia had a clinically stiff and edematous hindlimb, whereas those which had undergone 2 hr of ischemia and the sham animals had a normal hindlimb after 24 hr of reperfusion. PMN isolated from the venous effluent of an ischemic limb after 3 hr of ischemia and 24 hr of reperfusion demonstrated increased chemotaxis while systemic arterial PMN from the same animals showed no more chemotaxis than control cells. Regional changes in PMN continue to be present 24 hr after the injury and may contribute to an ongoing reperfusion injury despite adequate blood inflow being present.
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