OBJECTIVE: To evaluate the efficacy of nitric oxide (NO) inhalation against endotoxin-induced lung injury. DESIGN: Randomized prospective short-term study. SETTING: University school of Medicine Laboratory. INTERVENTIONS: Animal experiment (using 16 Japanese white rabbits). The animals inhaled NO at a concentration of 10 ppm. MEASUREMENTS AND RESULTS: The rabbits were randomly divided into the NO inhaling group (n = 7) and the control group (n = 9). Both groups received continuous infusion of 1200 mcg lipopolysaccharide (LPS) and the NO group inhaled 10 ppm NO during the LPS administration. In the control group, severe right ventricular (RV) failure was observed at 30-90 min of LPS infusion, and 4 of 9 animals died within 90 min of LPS infusion. In the NO group, none of the animals died and the early phase hemodynamic deterioration was milder than in the control group. But pulmonary gas exchange was not significantly different between the two groups throughout the study. At the end of the study there were no significant differences in any parameters of the surviving animals between the two groups. CONCLUSION: Although an improvement of pulmonary gas exchange was not demonstrated, NO inhalation (10 ppm) improved the outcome of severe RV failure caused by LPS infusion.
OBJECTIVE: To evaluate the efficacy of nitric oxide (NO) inhalation against endotoxin-induced lung injury. DESIGN: Randomized prospective short-term study. SETTING: University school of Medicine Laboratory. INTERVENTIONS: Animal experiment (using 16 Japanese white rabbits). The animals inhaled NO at a concentration of 10 ppm. MEASUREMENTS AND RESULTS: The rabbits were randomly divided into the NO inhaling group (n = 7) and the control group (n = 9). Both groups received continuous infusion of 1200 mcg lipopolysaccharide (LPS) and the NO group inhaled 10 ppm NO during the LPS administration. In the control group, severe right ventricular (RV) failure was observed at 30-90 min of LPS infusion, and 4 of 9 animals died within 90 min of LPS infusion. In the NO group, none of the animals died and the early phase hemodynamic deterioration was milder than in the control group. But pulmonary gas exchange was not significantly different between the two groups throughout the study. At the end of the study there were no significant differences in any parameters of the surviving animals between the two groups. CONCLUSION: Although an improvement of pulmonary gas exchange was not demonstrated, NO inhalation (10 ppm) improved the outcome of severe RV failure caused by LPS infusion.
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