Nitric oxide in critical respiratory failure of very low birth weight infants.

Abstract

Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator. In randomised trials, iNO increased gas exchange modestly and had no effect on the outcome (survival, chronic lung disease, CLD) in very low birth-weight (VLBW) infants. NO is an important component of the innate immune system and a lipid- soluble free radical scavenger that interacts with the surfactant system. VLBW infants with pneumonia and therapy-resistant, severe respiratory failure soon after birth were studied. Despite their infection, there was no detectable alveolar inducible NO synthase or nitrotyrosine, which is a toxic oxidation product of NO. These infants do not respond to exogenous surfactant and demonstrate severe pulmonary hypertension. However, they require exogenous surfactant prior to iNO. In most cases the disease is complicated by pneumonia and prolonged rupture of fetal membranes. We have shown evidence that iNO given within a few hours after birth reverses the progressive course of respiratory failure and pulmonary hypertension in VLBW infants.