Meconium Aspiration Delays Normal Decline of Pulmonary Vascular Resistance Shortly after Birth through Lung Parenchymal Injury

<i>Background:</i> Persistent pulmonary hypertension of the newborn is often associated with meconium aspiration syndrome (MAS) or perinatal asphyxia. <i>Objective:</i> To determine the effect of meconium or asphyxia on pulmonary arterial pressure and circulating levels of vasoactive substances, we conducted a prospective study of 54 term infants, including infants with meconium-stained amniotic fluid with normal (MSAF) or abnormal (MAS) chest X-ray findings, infants with perinatal asphyxia, and controls. The purpose of this study was to determine the group most likely to have elevated pulmonary arterial pressure and a disturbed balance between vasoactive substances. <i>Methods:</i> To estimate the pulmonary arterial pressure by echocardiography, we used the ratio of the right to left systolic ventricular pressure (RVP/LVP ratio). We measured the plasma concentrations of endothelin-1 (ET-1), cyclic guanosine monophosphate (cGMP) as an indicator of nitric oxide (NO) production, and 6-keto-prostaglandin F₁α (6-keto-PGF₁α) for the estimation of prostacyclin concentration. We also measured KL-6 as a marker of lung injury. <i>Results:</i>The RVP/LVP ratio was significantly higher in the MAS group than the other groups on day 0. Although ET-1 and 6-keto-PGF₁α levels were comparable among all groups, the cGMP level on days 3–5 and the KL-6 level throughout the first postnatal week were significantly higher in the MAS group. <i>Conclusions:</i> It is possible that meconium aspiration delays normal decline of pulmonary vascular resistance shortly after birth through lung parenchymal injury. The subsequent increase of cGMP in MAS may be an adaptive response to prevent further elevation of pulmonary arterial pressure by inducing NO.