ABSTRACT
Inhaled nitric oxide (iNO) is recognized as a potent and selective pulmonary vasodilator that does not decrease systemic vascular tone. The therapeutic application of iNO in human was first described in 1991. Subsequent reports showed that iNO therapy was effective to improve oxygenation in infants with persistent pulmonary hypertension of the newborn (PPHN). Owing to its selective pulmonary vasodilator effects, iNO therapy is an important treatment for term newborns with hypoxemic respiratory failure due to PPHN. The Food and Drug Administration of the United States of America first approved iNO in 1999 for use as a medical gas to treat hypoxic respiratory failure associated with clinical or echocardiographic evidence of pulmonary hypertension in term and late preterm neonates. Thereafter, iNO therapy is clinically applied to treat PPHN in term and late preterm neonates without consensus. In this review, we focused on the clinical practice of iNO therapy in PPHN. Based on published studies, we discuss iNO initiation and withdrawal methods, respiratory support devices that complement iNO therapy, and the patient and gas monitoring during iNO therapy.
Subject(s)
Female , Humans , Infant , Infant, Newborn , Americas , Complement System Proteins , Consensus , Echocardiography , Hypertension, Pulmonary , Nitric Oxide , Oxygen , Persistent Fetal Circulation Syndrome , Respiratory Insufficiency , United States , United States Food and Drug AdministrationABSTRACT
No abstract available.
Subject(s)
Adult , Aged , Humans , Middle Aged , Administration, Inhalation , Hemodynamics , Nitric Oxide/administration & dosage , Oxygen/blood , Positive-Pressure Respiration , Pulmonary Medicine , Respiratory Distress Syndrome/physiopathologyABSTRACT
PURPOSE: The aim of this study was to evaluate the effect of inhaled nitric oxide(iNO) on gas exchange, hemodynamics and pulmonary inflammation in newborn piglets with E. coli induced septic lung. METHODS: Twenty three instrumented and ventilated piglets were randomized into three groups: CON(n=6), PCON(n=9), and PNO(n=8). In the piglets of the PCON and PNO groups, E. coli septic lung was induced by endotracheal instillation of E. coli. Ten ppm iNO was given continuously in the PNO group after endotracheal instillation of E. coli. All animals were mechanically ventilated for six hour with a peak inspiratory pressure of 30 cmH2O, frequency of 25 breaths/min, FiO2 1.0 and a positive end-expiratory pressure of 4 cmH2O. All measurements were made at one hour intervals during the experiment. At the end of the experiment, lung tissue was harvested for the analysis of myeloperoxidase activity, indicative of lung inflammation. RESULTS: All piglets with pulmonary instillation of E. coli developed E. coli sepsis. Piglets in the PCON group developed progresseve pulmonry hypertension, hypoxemia and hypercarbia compared to the CON group due to increased pulmonary vascular resistance, intrapulmonary shunt fraction and physiologic dead space fraction. iNO did not reverse pulmonary hypertension in the PNO group. However iNO significantly improved oxygenation, which was attributed to marked improvement of venous admixture and partial attenuation of increase in dead space fraction. Increased myeloperoxidase activity in PCON compared to CON was significantly attenuated in PNO. CONCLUSION: iNO improves oxygenation and lung inflammation in newborn piglets with E. coli induced septic lung.