Meconium aspiration and birth asphyxia are both separately connected to significant pulmonary and systemic hemodynamic changes in newborns, but, although these insults frequently coexist, their combined effects on the neonatal circulation are still controversial. To determine the pulmonary and systemic circulatory changes induced by pulmonary meconium contamination with concurrent asphyxia, 41 anesthetized and ventilated newborn piglets (10 -12 d) were studied for 6 h. Eleven piglets were instilled with a bolus of human meconium intratracheally, and 10 piglets had meconium instillation with immediate induction of an asphyxic insult. Eight piglets had only asphyxia and 12 ventilated piglets served as controls. Meconium instillation (with and without asphyxia) resulted in a sustained decrease in the oxygenation, which remained, however, on the control level in the asphyxic group. Although meconium insufflation (with and without asphyxia) increased pulmonary artery pressure and vascular resistance progressively during the study period, the meconium-induced hypertensive effect was actually diminished by additional asphyxia. Asphyxia alone did not have any effect on these pulmonary hemodynamic parameters. On the other hand, whereas systemic arterial pressure and vascular resistance remained on the control level after meconium instillation alone, asphyxia (with and without pulmonary meconium insult) resulted in a sustained fall in systemic pressure already by 4 h. Our data thus indicate that although the coexisting asphyxia seems to moderate the meconium aspiration-induced pulmonary hypertensive response, this additional asphyxic insult does not affect the associated hypoxemia, but rather significantly exacerbates systemic hypotension. Abbreviations CO, cardiac output CVP, central venous pressure HR, heart rate MABP, mean arterial blood pressure MAS, meconium aspiration syndrome MPAP, mean pulmonary artery pressure PVR, pulmonary vascular resistance PWP, pulmonary wedge pressure SVR, systemic vascular resistance Aspiration of meconium-stained amniotic fluid frequently produces a severe respiratory failure in term and postterm infants. The clinical MAS has high morbidity and mortality, often linked with the presence of pulmonary hypertension (1-5). The pathophysiology and predisposing factors of the pulmonary hypertensive reaction in MAS are, however, complex and poorly defined. Although abnormal pulmonary arteriolar hypertrophy resulting from intrauterine hypoxia is supposed to play an etiologic role in some fatal cases of hypertensive MAS (6), experimental data indicate that acute intrapulmonary meconium contamination per se is able to cause, in a concentration-dependent manner, progressive pulmonary hypertensive response (2, 7). Alike, there are clinical data suggesting that meconium aspiration and its associated complications, rather than the structural vascular changes, are primarily responsible for the elevated pulmonary vasomotor tone and hypoxemic respiratory failure in newborns (8, 9). Because eventual disturb...