Editing Respiratory system (section)

===Other functions of the lungs===
====Local defenses====
Irritation of nerve endings within the [[nasal cavity|nasal passages]] or [[airway]]s, can induce a [[cough reflex]] and [[sneezing]]. These responses cause air to be expelled forcefully from the [[Vertebrate trachea|trachea]] or [[nose]], respectively. In this manner, irritants caught in the [[mucus]] which lines the respiratory tract are expelled or moved to the [[mouth]] where they can be [[swallowed]].<ref name=tortora1 /> During coughing, contraction of the smooth muscle in the airway walls narrows the trachea by pulling the ends of the cartilage plates together and by pushing soft tissue into the lumen. This increases the expired airflow rate to dislodge and remove any irritant particle or mucus.

[[Respiratory epithelium]] can secrete a variety of molecules that aid in the defense of the lungs. These include secretory [[immunoglobulin]]s (IgA), [[collectin]]s, [[defensin]]s and other peptides and [[proteases]], [[reactive oxygen species]], and [[reactive nitrogen species]]. These secretions can act directly as antimicrobials to help keep the airway free of infection. A variety of [[chemokine]]s and [[cytokine]]s are also secreted that recruit the traditional immune cells and others to the site of infections.

[[Pulmonary surfactant|Surfactant]] immune function is primarily attributed to two proteins: SP-A and SP-D. These proteins can bind to sugars on the surface of pathogens and thereby [[opsonize]] them for uptake by phagocytes. It also regulates inflammatory responses and interacts with the adaptive immune response. Surfactant degradation or inactivation may contribute to enhanced susceptibility to lung inflammation and infection.<ref>{{cite journal |doi=10.1159/000078172 |pmid=15211087 |title=Host Defense Functions of Pulmonary Surfactant |journal=Biology of the Neonate |volume=85 |issue=4 |pages=326–32 |year=2004 |last1=Wright |first1=Jo Rae |s2cid=25469141 }}</ref>

Most of the respiratory system is lined with mucous membranes that contain [[mucosa-associated lymphoid tissue]], which produces [[white blood cell]]s such as [[lymphocyte]]s.

====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>

====Contributions to whole body functions====
The lung vessels contain a [[Fibrinolysis|fibrinolytic system]] that dissolves [[Blood clots|clots]] that may have arrived in the pulmonary circulation by [[embolism]], often from the deep veins in the legs. They also release a variety of substances that enter the systemic arterial blood, and they remove other substances from the systemic venous blood that reach them via the pulmonary artery. Some [[prostaglandin]]s are removed from the circulation, while others are synthesized in the lungs and released into the blood when lung tissue is stretched.

The lungs activate one hormone. The physiologically inactive decapeptide [[angiotensin I]] is converted to the [[aldosterone]]-releasing octapeptide, [[angiotensin II]], in the pulmonary circulation. The reaction occurs in other tissues as well, but it is particularly prominent in the lungs. Angiotensin II also has a direct effect on [[Arteriole|arteriolar walls]], causing arteriolar [[vasoconstriction]], and consequently a rise in [[arterial blood pressure]].<ref>{{Cite journal|title = Cellular Mechanism of Vasoconstriction Induced by Angiotensin II It Remains To Be Determined|journal = Circulation Research|date = 2003-11-28|issn = 0009-7330|pmid = 14645130|pages = 1015–1017|volume = 93|issue = 11|doi = 10.1161/01.RES.0000105920.33926.60|language = en|first1 = Hideo|last1 = Kanaide|first2 = Toshihiro|last2 = Ichiki|first3 = Junji|last3 = Nishimura|first4 = Katsuya|last4 = Hirano|doi-access = free}}</ref> Large amounts of the [[angiotensin-converting enzyme]] responsible for this activation are located on the surfaces of the [[endothelial cells]] of the alveolar capillaries. The converting enzyme also inactivates [[bradykinin]]. Circulation time through the alveolar capillaries is less than one second, yet 70% of the angiotensin I reaching the lungs is converted to angiotensin II in a single trip through the capillaries. Four other peptidases have been identified on the surface of the pulmonary endothelial cells.

====Vocalization====
The movement of gas through the [[larynx]], [[pharynx]] and [[Human mouth|mouth]] allows humans to [[speech|speak]], or ''[[phonation|phonate]]''. Vocalization, or singing, in birds occurs via the [[Bird anatomy#Respiratory system|syrinx]], an organ located at the base of the trachea. The vibration of air flowing across the larynx ([[vocal cords]]), in humans, and the syrinx, in birds, results in sound. Because of this, gas movement is vital for [[communication]] purposes.

====Temperature control====
[[Thermoregulation|Panting]] in dogs, cats, birds and some other animals provides a means of reducing body temperature, by evaporating saliva in the mouth (instead of evaporating sweat on the skin).