Use of nitric oxide in meconium aspiration syndrome: lack of response

PURPOSE: To test the hypothesis that inhaled nitric oxide (INO) may not be an effective therapeutic agent in meconium aspiration syndrome (MAS). DESIGN: Prospective, interventional study. SETTING: The animal research laboratory at The Children's National Medical Center. SUBJECTS: Seven newborn pigs, 2-7 days old, weighing 2.8 +/- 0.17 kg were used for the study. MATERIALS AND METHODS: Animals were anaesthetized, paralysed, intubated and ventilated. Catheters were placed in the jugular vein, carotid artery, and pulmonary artery. After 1 h of recovery 10 ml/kg of 20% meconium in normal saline solution was insufflated into the lungs. Animals were ventilated to maintain ABGs in a normal range, i.e. pH = 7.35-7.45, PaCO2 = 40-45, and PaO2 = 70-90 torr. Ventilator settings were increased as needed until maximum settings of: FiO2 = 1.00, PIP = 40, IMV = 60. After 2 h of conventional ventilation or demonstration of significant lung disease by failure to maintain desired blood gases on maximum ventilator settings, INO was administered for 20 min in concentrations of 10, 20 and 40 ppm. To ensure that there was no additive effect of INO, a 15-min normalization period at 0 ppm was allowed between each dose of INO. Physiologic measurements, ventilatory settings, arterial blood gases, and methemoglobin were recorded at each study period. Measurements were taken after each exposure to INO and after its discontinuation. RESULTS: Arterial saturation (SaO2) and PaO2 were significantly lower ([81 +/- 18] and [54 +/- 14], respectively) and PAP was significantly higher [24 +/- 3] after MAS when compared with baseline. Administration of INO did not improve oxygenation nor decrease PAP at any of the study doses. CONCLUSION: In this model of MAS, short-term exposure to INO did not decrease PAP nor improve oxygenation. It may be postulated that poor distribution of INO caused by the obstructive nature of this disease may be responsible for the lack of response in this disease state, or that the primary etiology for hypoxia is parenchymal lung disease and not pulmonary hypertension.