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Am J Physiol Heart Circ Physiol 274: H1264-H1268, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 4, H1264-H1268, April 1998

Local L-NAME decreases blood flow and increases leukocyte adhesion via CD18

Debra J. Mitchell, Jingcheng Yu, and Karel Tyml

Department of Pharmacology and Toxicology and Department of Medical Biophysics, University of Western Ontario, and A. C. Burton Vascular Biology Lab, London Health Sciences Centre, London, Ontario, Canada N6A 5C1

Local inhibition of nitric oxide (NO) synthesis with L-arginine analogs such as NG-nitro-L-arginine methyl ester (L-NAME) decreased red blood cell velocity (VRBC) in capillaries and increased leukocyte adhesion in postcapillary venules in rat skeletal muscle. The goal of the present study was to determine the mechanism of this response to L-NAME. Using intravital videomicroscopy, we examined blood flow in the surface microvasculature of rat extensor digitorum longus muscle. L-NAME (30 mM in the pipette) locally applied to capillaries (300 µm from feeding arteriole) reduced VRBC [control VRBC = 244 ± 53 (SE) µm/s; Delta VRBC = -52 ± 8%] and increased leukocyte adhesion (from 0.2 ± 0.01 to 1.3 ± 0.3 cells/100 µm) in control animals. Systemic pretreatment with fucoidan (selectin binder), superoxide dismutase and catalase (extracellular antioxidants), dimethylthiourea (intracellular antioxidant), or ketotifen (mast cell stabilizer) did not alter this response. Pretreatment with CL26, an anti-CD18 antibody, abolished the L-NAME response. Our results suggest that L-NAME increased leukocyte-endothelial interactions via an effect on CD11/CD18 or its ligand, intercellular adhesion molecule.

capillary; nitric oxide; mast cells


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