title: Inhaled NO reduces leukocyte-endothelial cell interactions and myocardial dysfunction in endotoxemic rats.
abstract: Inhaled nitric oxide (NO) has been shown to have some protective effect in the peripheral distal inflamed vasculature. The objective of the study was to determine whether inhaled NO would reduce endotoxin-induced leukocyte activation and myocardial contractile dysfunction. Rats were treated with either saline or endotoxin (10 mg/kg iv) and then allowed to breathe (4 h) either air or air plus NO (10 ppm). In endotoxemic rats, mesenteric venular endothelium leukocyte firm adhesion increased compared with control rats (1.15 +/- 0.32 vs. 4.08 +/- 0.96 leukocytes/100 microm; P < 0.05). Inhaled NO significantly attenuated endotoxin-induced venular endothelium leukocyte adhesion (4.08 +/- 0.96 vs. 1.86 +/- 0.76 leukocytes/100 microm; P < 0.05) and FITC-conjugated anti-intercellular adhesion molecule-1 fluorescence intensity. Endotoxin-induced myocardial dysfunction and leukocyte content increases were reduced in inhaled NO-treated rats. These observations suggest that inhaled NO reduces the degree of cardiovascular dysfunction and inflammation in endotoxemic rats.
authors.affiliation: Réanimation Médicale, Hopital Calmette, Hopital Huriez, Centre Hospitalier Universitaire Lille 59037, France. rneviere@univ-lille2.fr
authors.forename: R
authors.initials: R
authors.lastname: Nevière
authors.forename: B
authors.initials: B
authors.lastname: Guery
authors.forename: S
authors.initials: S
authors.lastname: Mordon
authors.forename: F
authors.initials: F
authors.lastname: Zerimech
authors.forename: S
authors.initials: S
authors.lastname: Charré
authors.forename: F
authors.initials: F
authors.lastname: Wattel
authors.forename: C
authors.initials: C
authors.lastname: Chopin
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D019446:Endotoxemia / Q000503:physiopathology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects / Q000378:metabolism; D007962:Leukocytes / Q000502:physiology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009569:Nitric Oxide / Q000494:pharmacology*; D010088:Oxidoreductases / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013152:Splanchnic Circulation; D016277:Ventricular Function, Left; D014699:Venules / Q000473:pathology
chemical_list: D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide; D010088:Oxidoreductases; D009195:Peroxidase