RENAL ISCHEMIC-REPERFUSION INJURY IN L-SELECTIN-DEFICIENT MICE

L-selectin an leukocyte surfaces mediates cell rolling on endothelium. L-selectin blockade with antibodies attenuated ischemic-reperfusian i njury (IRI) in heart and skeletal muscle, but its role in renal IRI is unknown. We evaluated the role of L-selectin in renal IRI using L-sel ectin-deficient mice. Neutrophil migration to chemically inflamed peri toneum was reduced by 47% (P < 0.01) in L-selectin-deficient mice. Isc hemia was induced by bilateral renal pedicle clamping for 30 min. Cont rol and L-selectin groups had similar elevations of serum creatinine ( 1.8 +/- 0.3 vs. 1.7 +/- 0.2 mg/dl) and blood urea nitrogen (111 +/- 17 vs. 128 +/- 12 mg/dl) 24 h postischemia. Pathological assessment show ed comparable degrees of tubular necrosis at 24 h. The postischemic in crease in peritubular neutrophils per 10 high-power fields was similar in control and L-selectin-deficient groups at 4 (28 +/- 10 vs. 22 +/- 5), 12 (245 +/- 80 vs. 236 +/- 78), and 24 h (130 +/- 12 vs. 156 +/- 18). These data argue against a significant role for L-selectin in ren al IRI. Pathophysiological roles of L-selectin in vivo appear to be mo re complex than in vitro data would suggest.