Effect of inhaled nitric oxide on pulmonary function after sepsis in a swine model

H. Ogura, W. G. Cioffi*, P. J. Offner, B. S. Jordan, A. A. Johnson, B. A. Pruitt, F. A. Moore, T. Billiar, K. Messmer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

46 Scopus citations


Background. Inhaled nitric oxide (NO) has been shown to improve sepsis induced pulmonary dysfunction. This study evaluated the mechanism by which inhaled NO improves pulmonary function in a porcine sepsis model. Methods. After an infusion of Escherichia coli lipopolysaccharide (LPS, 200 μg/kg), animals were resuscitated with saline solution (1 ml/kg/min) and observed for 3 hours while mechanically ventilated, (fraction of inspired oxygen, 0.6; tidal volume, 12 ml/kg; positive end-expiratory pressure, 5 cm H2O). Group 1 (LPS, n = 6) received no additional treatment. Group 2 (NO, n = 6) received inhaled NO (40 ppm) for the last 2 hours. Group 3 (control, n = 5) received only saline solution without LPS. Cardiopulmonary variables and blood gases were measured serially. Multiple inert gas elimination technique was performed at 3 hours. Wet to dry lung weight ratio was measured after necropsy. Results. Lipopolysaccharide resulted in pulmonary arterial hypertension, pulmonary edema, and hypoxemia. Multiple inert gas elimination technique analysis indicated a significant increase in blood flow to true shunt and high ventilation perfusion distribution (V(A)/Q) areas with an increased dispersion of V(A)/Q distribution. All of these changes were significantly attenuated by NO. Conclusions. Inhaled NO significantly improved LPS induced V(A)/Q mismatching by decreasing both true shunt and high V(A)/Q areas, by decreasing pulmonary edema, and by redistributing blood flow from true shunt to ventilated areas.

Original languageEnglish
Pages (from-to)313-321
Number of pages9
Issue number2
StatePublished - 1994
Externally publishedYes


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