Editing Meconium aspiration syndrome (section)

=== Antiinflammatories ===
As inflammation is such a huge issue in MAS, treatment has consisted of anti-inflammatories.

==== Glucocorticoids ====
[[Glucocorticoid]]s have a strong anti-inflammatory activity and works to reduce the migration and activation of [[neutrophil]]s, [[eosinophil]]s, [[Monocyte|mononuclear]] cells, and other cells. They reduce the migration of neutrophils into the lungs ergo, decreasing their adherence to the [[endothelium]]. Thus, there is a reduction in the action of mediators released from these cells and therefore, a reduced inflammatory response.<ref name=":11">{{Cite journal|last1=Mokra|first1=D|last2=Mokry|first2=J|date=2011|title=Glucocorticoids in the Treatment of Neonatal Meconium Aspiration Syndrome|journal=Eur J Pediatr|volume=170|issue=12|pages=1495–1505|doi=10.1007/s00431-011-1453-2|pmc=3221844|pmid=21465122}}</ref><ref name=":7" />

Glucocorticoids also possess a genomic mechanism of action in which, once bound to a [[glucocorticoid receptor]], the activated complex moves into the [[Cell nucleus|nucleus]] and inhibits [[Transcription (biology)|transcription]] of [[Messenger RNA|mRNA]]. Ultimately, effecting whether various proteins get produced or not. Inhibiting the transcription of nuclear factor ([[NF-κB]]) and protein activator ([[AP-1 transcription factor|AP-1]]) attenuates the expression of pro-inflammatory cytokines ([[Interleukin-1 family|IL-1]], [[Interleukin 6|IL-6]], [[Interleukin 8|IL-8]] and [[Tumor necrosis factor superfamily|TNF]] etc.), enzymes ([[Phospholipase A2|PLA<sub>2</sub>]], [[Cyclooxygenase-2|COX-2]], [[Nitric oxide|iNOs]] etc.) and other biologically active substances.<ref name=":12">{{Cite journal|last1=Czock|first1=D|last2=Keller|first2=F|last3=Rasche|first3=FM|last4=Haussler|first4=U|date=2005|title=Pharmacokinetics and Pharmacodynamics of Systemically Administered Glucocorticoids|journal=Clinical Pharmacokinetics|volume=44|issue=1|pages=61–98|doi=10.2165/00003088-200544010-00003|pmid=15634032|s2cid=24458998}}</ref><ref name=":11" /><ref name=":7" /> The anti-inflammatory effect of glucocorticoids is also demonstrated by enhancing the activity of lipocortines which inhibit the activity of PLA<sub>2</sub> and therefore, decrease the production of [[arachidonic acid]] and mediators of [[lipoxygenase]] and [[cyclooxygenase]] pathways.<ref name=":11" />

[[Anti-inflammatory|Anti-inflammatories]] need to be administered as quickly as possible as the effect of these drugs can diminish even just an hour after meconium aspiration. For example, early administration of [[dexamethasone]] significantly enhanced [[gas exchange]], reduced ventilatory pressures, decreased the number of [[neutrophil]]s in the bronchoalveolar area, reduced [[Edema|oedema]] formation and oxidative lung injury.<ref name=":7" /> However, glucocorticoids may increase the risk of infection and this risk increases with the dose and duration of glucocorticoid treatment. Other issues can arise, such as aggravation of [[diabetes mellitus]], [[osteoporosis]], skin [[atrophy]] and [[growth retardation]] in children.<ref name=":12" />

==== 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>

==== Inhibitors of cyclooxygenase ====
[[Arachidonic acid]] is metabolised, via [[cyclooxygenase]] (COX) and [[lipoxygenase]], to various substances including [[prostaglandin]]s and [[leukotriene]]s, which exhibit potent pro-inflammatory and [[Vasoactivity|vasoactive]] effects. By inhibiting COX, and more specifically [[COX-2]], (either through selective or non-selective drugs) inflammation and oedema can be reduced. However, COX inhibitors may induce [[Peptic ulcer disease|peptic ulcers]] and cause [[hyperkalemia]] and [[hypernatremia]]. Additionally, COX inhibitors have not shown any great response in the treatment of MAS.<ref name=":7" />