Editing Respiratory system (section)

====Prevention of alveolar collapse====
{{Main|Pulmonary surfactant}}
The lungs make a [[pulmonary surfactant|surfactant]], a surface-active [[lipoprotein]] complex (phospholipoprotein) formed by [[Type II pneumocyte|type II alveolar cells]]. It floats on the surface of the thin watery layer which lines the insides of the alveoli, reducing the water's surface tension.

The surface tension of a watery surface (the water-air interface) tends to make that surface shrink.<ref name=tortora1 /> When that surface is curved as it is in the alveoli of the lungs, the shrinkage of the surface decreases the diameter of the alveoli. The more acute the curvature of the water-air interface [[Pulmonary surfactant#Function|the greater the tendency for the alveolus to collapse]].<ref name=tortora1 /> This has three effects. Firstly, the surface tension inside the alveoli resists expansion of the alveoli during inhalation (i.e. it makes the lung stiff, or non-compliant). Surfactant reduces the surface tension and therefore makes the lungs more [[Pulmonary compliance|compliant]], or less stiff, than if it were not there. Secondly, the diameters of the alveoli increase and decrease during the breathing cycle. This means that the alveoli have a [[Pulmonary surfactant#Compliance|greater tendency to collapse]] (i.e. cause [[atelectasis]]) at the end of exhalation than at the end of inhalation. Since surfactant floats on the watery surface, its molecules are more tightly packed together when the alveoli shrink during exhalation.<ref name=tortora1 /> This causes them to have a greater surface tension-lowering effect when the alveoli are small than when they are large (as at the end of inhalation, when the surfactant molecules are more widely spaced). The tendency for the alveoli to collapse is therefore almost the same at the end of exhalation as at the end of inhalation. Thirdly, the surface tension of the curved watery layer lining the alveoli tends to draw water from the lung tissues into the alveoli. Surfactant reduces this danger to negligible levels, and keeps the alveoli dry.<ref name=tortora1 /><ref>{{cite book|author=West, John B.|title=Respiratory physiology-- the essentials|publisher=Williams & Wilkins|location=Baltimore|year=1994|pages=[https://archive.org/details/respiratoryphysi00west/page/21 21–30, 84–84, 98–101]|isbn=0-683-08937-4|url=https://archive.org/details/respiratoryphysi00west/page/21}}</ref>

[[Premature birth|Pre-term babies]] who are unable to manufacture surfactant have lungs that tend to collapse each time they breathe out. Unless treated, this condition, called [[Infant respiratory distress syndrome|respiratory distress syndrome]], is fatal. Basic scientific experiments, carried out using cells from chicken lungs, support the potential for using [[steroid]]s as a means of furthering the development of type II alveolar cells.<ref>{{cite journal|pmid=11506991 |year=2001|last1=Sullivan|first1=LC|last2=Orgeig|first2=S|title=Dexamethasone and epinephrine stimulate surfactant secretion in type II cells of embryonic chickens|volume=281|issue=3|pages=R770–7|journal=American Journal of Physiology. Regulatory, Integrative and Comparative Physiology|doi=10.1152/ajpregu.2001.281.3.r770|s2cid=11226056 }}</ref> In fact, once a [[Preterm birth|premature birth]] is threatened, every effort is made to delay the birth, and a series of [[steroid]] injections is frequently administered to the mother during this delay in an effort to promote lung maturation.<ref>[https://web.archive.org/web/20070604020429/http://www.pregnancy-facts.com/articles/childbirth/premature-babies.php Premature Babies, Lung Development & Respiratory Distress Syndrome]. Pregnancy-facts.com.</ref>