Editing Meconium aspiration syndrome (section)

==== Inhibitors of phosphodiesterase ====
[[Phosphodiesterase]]s (PDE) degrades [[Cyclic adenosine monophosphate|cAMP]] and [[Cyclic guanosine monophosphate|cGMP]] and, within the [[respiratory system]] of a newborn with MAS, various isoforms of PDE may be involved due to their pro-inflammatory and [[Smooth muscle tissue|smooth muscle]] contractile activity. Therefore, non-selective and selective inhibitors of PDE could potentially be used in MAS therapy. However, the use of PDE inhibitors can cause [[cardiovascular]] side effects. Non-selective PDE inhibitors, such as [[methylxanthines]], increase concentrations of cAMP and cGMP in the cells leading to [[Bronchodilator|bronchodilation]] and [[vasodilation]]. Additionally, methylxanthines decreases the concentrations of calcium, [[acetylcholine]] and [[monoamines]], this controls the release of various mediators of inflammation and [[bronchoconstriction]], including [[prostaglandin]]s. Selective PDE inhibitors target one subtype of [[phosphodiesterase]] and in MAS the activities of [[Phosphodiesterase 3|PDE-3]], [[Phosphodiesterase 4|PDE-4]], [[Phosphodiesterase 5|PDE-5]] and PDE-7 may become enhanced.<ref name=":7" /> For example, [[Milrinone]] (a selective PDE3 inhibitor) improved oxygenation and survival of neonates with MAS.<ref>{{Cite journal|last1=Bassler|first1=D|last2=Choong|first2=K|last3=McNamara|first3=P|last4=Kirpalani|first4=H|date=2006|title=Neonatal Persistent Pulmonary Hypertension Treated with Milrinone: Four Case Report|journal=Biology of the Neonate|volume=89|issue=1|pages=1–5|doi=10.1159/000088192|pmid=16155380|s2cid=38587541}}</ref>