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  • Title: L-NAME-induced neutrophil accumulation in rat lung is not entirely because of interactions with L- and P-selectins or CD18.
    Author: Roman A, McGahren ED.
    Journal: J Pediatr Surg; 2006 Oct; 41(10):1743-9. PubMed ID: 17011281.
    Abstract:
    BACKGROUND/PURPOSE: Nitric oxide (NO) is a known selective dilator of the pulmonary vascular tree. There is evidence that it also plays a role in diminishing neutrophil adherence to vascular endothelial cells. Close examination of these effects of NO on the pulmonary microcirculation is essential to our understanding of its mechanisms of action as well as its potential as a therapeutic agent to reduce neutrophil sequestration, and its subsequent damage, in a variety of conditions that cause lung injury and inflammation. This study explores the mechanism by which endogenous NO influences neutrophil-endothelial cell interactions by examining the effects of the adhesion molecule blockers, fucoidin, and anti-CD18 antibody. METHODS: Lung samples from 10 sets of rats (n = 4 for each study group) were studied. Each rat received an intravenous bolus of normal saline, fucoidin, or anti-CD18 antibody, followed by a 1-hour infusion of normal saline or N omega-nitro-L-arginine methyl ester (L-NAME) at 2 mg kg(-1) min(-1). The accumulation of neutrophils within the lungs was assessed quantitatively by myeloperoxidase assay. RESULTS: Fucoidin application decreased some neutrophil activity, but this may have been independent of the effects on L-NAME activity. The anti-CD18 pretreatment did not have a significant effect on any of the groups in the presence or absence of L-NAME. CONCLUSIONS: These data indicate that L-NAME does not conclusively produce its associated increase in neutrophil activity in the baseline state of the lungs via an interaction with L-selectin, P-selectin, or CD18. Rather, the inhibition of NO may lead to the expression of a different adhesion molecule or factor that is normally not expressed in the presence of NO. Endogenous NO may also possibly influence neutrophil-endothelial interaction by affecting hemodynamics rather than actions of adhesion molecules.
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