EFFECTS OF INHALED NITRIC-OXIDE DURING PERMISSIVE HYPERCAPNIA IN ACUTE RESPIRATORY-FAILURE IN PIGLETS

Objective: To look for the effects of inhaled nitric oxide on oxygenat ion and pulmonary hemodynamics during acute hypercapnia in acute respi ratory failure, Design: Prospective, randomized, experimental study, S etting: University research laboratory. Subjects: Ten piglets, weighin g 9 to 13 kg, Interventions: Acute respiratory failure was induced by oleic acid infusion and repeated lung lavages with 0.9% sodium chlorid e, The protocol consisted of three randomly assigned periods with diff erent Paco(2) levels, Tidal volume was reduced to induce hypercapnia. Inspiratory time was prolonged to achieve similar mean airway pressure s, During permissive hypercapnia, pH was not corrected, At each Paco(2 ) period, the animals were ventilated with inhaled nitric oxide of 10 parts per million and without nitric oxide inhalation. Measurements an d Main Results: Continuous hemodynamic monitoring included right atria l, mean pulmonary arterial, and mean systemic arterial pressures, arte rial and mixed venous oxygen saturations, and continuous flow recordin g at the pulmonary ar tery, In addition, airway pressures, tidal volum es, dynamic lung compliance and airway resistance, end-tidal CO2 conce ntrations, and arterial and mixed venous blood gases were measured. Da ta were obtained at baseline and after lung injury, at normocapnia, at two levels of hypercapnia with and without nitric oxide inhalation. A cute hypercapnia resulted in a significant decrease in blood pH and a significant increase in mean pulmonary arterial pressure. There was no significant change in Pao(2) during normocapnia and hypercapnia, Inha led nitric oxide significantly decreased the mean pulmonary arterial p ressure during both hypercapnic periods, It significantly improved oxy genation during both normocapnia and hypercapnia. Conclusions: Acute h ypercapnia resulted in a significant increase in pulmonary arterial pr essure without influencing oxygenation and cardiac output, Inhaled nit ric oxide significantly reduced the pulmonary hypertension induced by acute permissive hypercapnia but did not influence the flow through th e pulmonary artery, Inhaled nitric oxide significantly improved oxygen ation in this model of acute lung injury during normocapnia and acute hypercapnia.