Renal ischemic-reperfusion injury in l-selectin deficient mice.
Rabb, Hamid, German Ramirez, Sabiha R. Saba, Daniel Reynolds, Jianchao
Xu, Richard Flavell & Scott Antonia.
Departments of Medicine and Pathology, University of South Florida,
James A. Haley VA Hospital & H. Lee Moffitt Cancer Center, Tampa,
Florida 33612, Howard Hughes Medical Institute, Yale University
School of Medicine, New Haven, Connecticut 06510
APStracts 3:0066F, 1996.
L-selectin on leukocyte surfaces mediates cell rolling on endothelium.
L- selectin blockade with antibodies attenuated ischemic reperfusion
injury (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
-selectin deficient mice. Neutrophil migration to chemically inflamed
peritoneum was reduced by 47% (p<0.01) in L-selectin deficient
mice. Ischemia was induced by bilateral renal pedicle clamping for 30
minutes. 24 hour post- ischemia, control and L-selectin groups had
similar elevations of serum creatinine (1.8 + 0.3 mg/dl vs. 1.7 + 0.2
mg/dl) and blood urea nitrogen (111 + 17 mg/dl vs. 128 + 12 mg/dl).
Pathologic assessment showed comparable degrees of tubular necrosis
at 24 hours. The postischemic increase in peri-tubular neutrophils/10
HPF was similar in control and L- selectin deficient groups at 4 (28
+ 10 vs 22 + 5), 12 (245 + 80 vs 236 + 78) and 24 hours (130 + 12 vs
156 + 18). These data argue against a significant role for L-selectin
in renal IRI. Pathophysiologic roles of L- selectin in vivo appear to
be more complex than in vitro data would suggest.
Received 27 October 1995; accepted in final form 15 March 1996.
APS Manuscript Number F366-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96