engleski

Nitric oxide in neonatology

Persistent pulmonary hypertension (PPHN) of the neonate is a frustrating and sometimes lethal cardiorespiratory complication of the transition to extrauterine life. It is characterised by pulmonary hypertension and extra pulmonary right-to-left shunting across the formanmen ovale and ductus arterioles. PPHN is frequently associated with pulmonary parenchymal abnormalities, including meconium aspiration, pneumonia, sepsis, and lung hypoplasia. In some instances, there is no evidence of pulmonary parenchymal disease and the aetiology is unknown. In many cases, the disease progressively worsens, becoming refractory to treatment. Despite the availability of potent vasodilators such as tolasoline, prostaglandin E, and nitroprusside and their efficiency in lowering pulmonary vascular resistance, their use is severely limited by lack of pulmonary selectivity. Systemic vasodilatation invariably occurs, leading to hypotension, compromised tissue perfusion, and inadequate oxygen delivery to vital organs. When other therapies fail, neonates are treated with extracorporeal membrane oxygenation (ECMO) which improves survival but its administration is labor- intensive and costly, causes important morbidity, and is unavailable at many intensive care nurseries. The discovery that nitric oxide mediates endothelium- derived relaxation of pulmonary vessels is of paramount importance. Inhaled nitric oxide (iNO) does not cause systemic hypotension when it diffuses into the intravascular space, because it is inactivated by avid binding to haemoglobin. iNO is, at present, the only effective, selective, pulmonary vasodilator therapy which has been consistently proved efficacious in the multiple large randomized clinical trials.

nitric oxide ; persistent pulmonary hypertension ; neonate

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