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1 Réanimation Médicale, Hopital Calmette; 2 EA 2689 Institut National de la Sant é et de la Recherche Médicale; and 3 Service de Biochimie, Hopital Huriez, Centre Hospitalier Universitaire Lille 59037, France
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 µm; P < 0.05). Inhaled NO significantly attenuated endotoxin-induced venular endothelium leukocyte adhesion (4.08 ± 0.96 vs. 1.86 ± 0.76 leukocytes/100 µm; 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.
left ventricular function; microcirculation; endotoxin; nitric oxide inhalation
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