Abstract 9779: Nitric Oxide Generated Through Ascorbic Acid Reduction of Nitrogen Dioxide Reduces Pulmonary Vascular Resistance in Hypoxemic Swine with Minimal Inhaled and Exhaled Nitrogen Dioxide
Background: Inhaled nitric oxide (NO) has the capacity to selectively dilate pulmonary blood vessels and improve oxygenation in patients with pulmonary diseases. NO in the presence of oxygen spontaneously converts to nitrogen dioxisw (NO2), a toxic byproduct with multiple adverse pulmonary effects. The potential for co-inhalation of NO2 drives delivery system complexity, gas monitoring and cost. We demonstrate a new method for generating inhaled NO based on reducing NO2 just prior to inhalation, using ascorbic acid/silica gel reactor cartridges (GeNO, LLC). Ascorbic acid protonates NO2, yielding NO, water and dehydroascorbic acid. This reaction occurs within the ventilator hoses, leaving little time for NO2 reformation.
Methods: In vivo efficacy was assessed through the inhalation of NO (1, 5, 20, and 80 PPM) in hypoxemic swine (FiO2 15%). NO2 in N2 was mixed with O2 prior to entry into the hoses of a portable ventilator upstream of two ascorbic acid cartridges in series. Inhaled and exhaled NO and NO2 were sampled using in-line electrochemical detectors (step response time < 0.8 s, GeNO, LLC).
Results: Inspired and expired NO2 was always under 0.3 PPM in 50% and 0.9 PPM in 100% O2 (Fig. 1). Inhaled NO significantly reduced the hypoxemia elevated mean pulmonary artery pressure and pulmonary vascular resistance at all doses (Fig. 2).
Conclusion: Inspired and even expired NO2 levels were low using ultra-fast electrochemical methods. NO supplied by this novel system was capable of reversing hypoxemia induced pulmonary hypertension. The lack of co-delivered toxic NO2 may allow for a substantial reconsideration of the therapeutic role of inhaled NO in a wide range of respiratory diseases.
- © 2011 by American Heart Association, Inc.