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Am J Physiol Lung Cell Mol Physiol 274: L337-L342, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 3, L337-L342, March 1998

L-Arginine prevents lung neutrophil accumulation and preserves pulmonary endothelial function after endotoxin

Brett C. Sheridan1, Robert C. McIntyre Jr.1, Daniel R. Meldrum1, and David A. Fullerton2

1 Department of Surgery, University of Colorado, Denver, Colorado 80262; and 2 Department of Surgery, Northwestern University, Chicago, Illinois 60611

L-Arginine supplementation has been shown to restore endothelium-derived nitric oxide production in several pathological states. The purpose of this study was to examine the effect of administration of exogenous L-arginine on the endotoxin-induced lung neutrophil accumulation and impairment of endothelium-dependent guanosine 3',5'-cyclic monophosphate (cGMP)-mediated pulmonary vasorelaxation in rats. Endothelium-dependent relaxation was tested by receptor-dependent [acetylcholine (ACh)] and receptor-independent (A-23187) pathways. Endothelium-independent relaxation was tested with sodium nitroprusside (SNP). In isolated pulmonary arterial rings, concentration-response curves were generated with ACh, A-23187, and SNP (10-9 to 10-6 M) 4 h after endotoxin (500 µg/kg ip) with and without prior administration of L-arginine (300 mg/kg ip). Lung neutrophil accumulation was determined by myeloperoxidase (MPO) assay. After endotoxin, lung neutrophil accumulation was significantly increased (MPO activity, 3.8 ± 0.4 vs. 0.8 ± 0.1 units/g lung weight in control cells; P < 0.05), which was prevented by L-arginine treatment (MPO activity, 1.3 ± 0.3 units/g lung weight; P < 0.05 vs. endotoxin). Endotoxin produced a significant impairment of endothelium-dependent cGMP-mediated pulmonary vasorelaxation by receptor-dependent (ACh) and -independent (A-23187) pathways as well as of endothelium-independent relaxation (SNP). Prior treatment with L-arginine, but not with D-arginine, preserved endothelium-dependent vasorelaxation. Neither L- nor D-arginine influenced endotoxin-induced impairment of endothelium-independent, cGMP-mediated pulmonary vasorelaxation. We conclude that administration of exogenous L-arginine prevents endotoxin-induced lung neutrophil accumulation and attenuates its associated impairment of endothelium-dependent, cGMP-mediated pulmonary vasorelaxation.

vasorelaxation


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