Nitric oxide inhalation increases alveolar gas exchange by decreasing deadspace volume

Objective: To test the hypothesis that nitric oxide inhalation facilitates CO2 elimination by decreasing alveolar deadspace in an ovine model of acute lung injury. Design: Prospective, placebo-controlled, randomized, crossover model. Setting: University research laboratory. Subjects: Eleven mixed-breed adult sheep. Interventions: To induce acute lung injury, hydrochloric acid was instilled into the tracheas of paralyzed sheep receiving controlled mechanical venti lation. Each sheep breathed 0 ppm, 5 ppm, and 20 ppm nitric oxide in random order. Measurements and Main Results: Estimates of alveolar deadspace volumes and arterial-to-end tidal CO(2)partial pressure differences were used as indica tors of CO2 elimination efficiency. At a constant minute ventilation, nitri c oxide inhalation caused dose-independent decreases in Pace, (p < .05), al veolar dead- space (p < .01), and arterial-to-end tidal CO2 partial pressur e differences (p < .01). We found that estimates of arterial-to-end tidal C O2 partial pressure differences may be used to predict alveolar deadspace v olume (r(2) =.86, p < .05), Conclusions: Estimates of arterial-to-end tidal CO2 partial pressure differ ences are reliable indicators of alveolar deadspace. Both values decreased during nitric oxide inhalation in our model of acutely injured lungs. This finding supports the idea that nitric oxide inhalation facilitates CO2 elim ination in acutely injured lungs. Future studies are needed to determine wh ether nitric oxide therapy can be used to reduce the work of breathing in s elected patients with cardiopulmonary disorders,