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Alveolar Gas Equation - Part 2
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RESULTS [51 .. 101]
From Wikipedia, the free encyclopedia
  (Redirected from Alveolar)
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"Alveolus" redirects here. For other uses, see Alveolus (disambiguation).
"Alveolar" redirects here. For the consonant class, see Alveolar consonant.
"Air sac" redirects here. For the specialist air sacs found in birds, see bird anatomy. For the air sac in the throat of birds and other species, see throat sac.
Pulmonary alveolus
Alveolus diagram.svg
The alveoli
Latin alveolus pulmonis
Code TH H3.05.02.0.00026

An alveolus (plural: alveoli, from Latin alveolus, "little cavity") is an anatomical structure that has the form of a hollow cavity.[1] Found in the lung parenchyma, the pulmonary alveoli are the terminal ends of the respiratory tree, which outcrop from either alveolar sacs or alveolar ducts, which are both sites of gas exchange with the blood as well.[2] Alveoli are particular to mammalian lungs. Different structures are involved in gas exchange in other vertebrates.[3] The alveolar membrane is the gas-exchange surface. Carbon dioxide rich blood is pumped from the rest of the body into the alveolar blood vessels where, through diffusion, it releases its carbon dioxide and absorbs oxygen.[4]

Structure[edit]

The alveoli are located in the respiratory zone of the lungs, at the distal termination of the alveolar ducts and atria. These air sacs are the forming and termination point of the respiratory tract. They provide total surface area of about 100 m2.[5]

Bronchial anatomy

A typical pair of human lungs contain about 700 million alveoli,[6] producing 70m2 of surface area.[7] Each alveolus is wrapped in a fine mesh of capillaries covering about 70% of its area. An adult alveolus has an average diameter of 200 micrometres, with an increase in diameter during inhalation.[8]

The alveoli consist of an epithelial layer and extracellular matrix surrounded by capillaries. In some alveolar walls there are pores between alveoli called Pores of Kohn. The alveoli contain some collagen and elastic fibres. The elastic fibers allow the alveoli to stretch as they are filled with air during inhalation. They then spring back during exhalation in order to expel the carbon dioxide-rich air.

Histology[edit]

There are three major cell types in the alveolar wall (pneumocytes):

  • Type I (Squamous Alveolar) cells that form the structure of an alveolar wall
  • Type II (Great Alveolar) cells that secrete pulmonary surfactant to lower the surface tension of water and allows the membrane to separate, therefore increasing its capability to exchange gases. Surfactant is continuously released by exocytosis. It forms an underlying aqueous protein-containing hypophase and an overlying phospholipid film composed primarily of dipalmitoyl phosphatidylcholine.
  • Macrophages that destroy foreign material, such as bacteria.

Reinflation of the alveoli following exhalation is made easier by pulmonary surfactant, which is a phospholipid and protein mixture that reduces surface tension in the thin fluid coating within all alveoli. The fluid coating is produced by the body in order to facilitate the transfer of gases between blood and alveolar air. The surfactant is produced by great alveolar cells (granular pneumonocytes, a cuboidal epithelia), which are the most numerous cells in the alveoli, yet do not cover as much surface area as the squamous alveolar cells (a squamous epithelium).

Great alveolar cells also repair the endotheilium of the alveolus when it becomes damaged. Insufficient pulmonary surfactant in the alveoli can contribute to atelectasis (collapse of part or all of the lung). Without pulmonary surfactant, atelectasis is a certainty; however, there are other causes of lung collapse such as trauma (pneumothorax), COPD, and pleuritis.[9]

Clinical significance[edit]

Diseases[edit]

Main article: Respiratory disease
  • In asthma, the bronchioles, or the "bottle-necks" into the sac are restricted, causing the amount of air flow into the lungs to be greatly reduced. It can be triggered by irritants in the air, photochemical smog for example, as well as substances that a person is allergic to.
  • Emphysema is another disease of the lungs, whereby the elastin in the walls of the alveoli is broken down by an imbalance between the production of neutrophil elastase (elevated by cigarette smoke) and alpha-1-antitrypsin (the activity varies due to genetics or reaction of a critical methionine residue with toxins including cigarette smoke). The resulting loss of elasticity in the lungs leads to prolonged times for exhalation, which occurs through passive recoil of the expanded lung. This leads to a smaller volume of gas exchanged per breath.
  • Chronic bronchitis occurs when an abundance of mucus is produced by the lungs. The production of this substance occurs naturally when the lung tissue is exposed to irritants. In chronic bronchitis, the air passages into the alveoli, the broncholiotes, become clogged with mucus. This causes increased coughing in order to remove the mucus, and is often a result of extended periods of exposure to cigarette smoke.
  • Cystic fibrosis is a genetic condition. A mutation of the cystic fibrosis transmembrane conductance regulator gene causes defective CFTR proteins, which are transmembrane proteins that function in Cl transport in wet epithelia. Because wet epithelium is such a ubiquitous and multipurpose tissue type, CF has myriad deleterious effects, some of the most serious of which are severe respiratory problems. Many of the mechanisms by which CF causes damage or inadequate function in the wet epithelia of other tissues, such as the digestive and reproductive tracts, are well-understood. CF's mechanisms in causing lung disease, however, remain poorly elucidated. One popular hypothesis suggests increased viscosity due to increased salinity of the mucous secreted by glands of the pseudostratified respiratory epithelium, causing difficulty in maintaining normal respiratory tract mucociliary clearance. The frequency of certain specific bacterial infections (Pseudomonas, Haemophilus influenzae, Staphylococcus) has prompted two other popular categories of hypotheses: that the high salt content may interfere with defensins and lysosome, and/or may encourage the growth of the several bacterial species typically infecting the ordinarily-sterile lower lungs of CF patients. Regular treatment is usually required—primarily percussive therapy and antibiotics. Promising research into gene therapies is taking place.
  • Lung cancer is a common form of cancer causing the uncontrolled growth of cells in the lung tissue. Due to the sensitivity of lung tissue, such malignant growth is often hard to treat effectively.
  • Pneumonia is an infection of the lung parenchyma, which can be caused by both viruses and bacteria. Cytokines and fluids are released into the alveolar cavity and/or interstitium in response to infection, causing the effective surface area of gas exchange in the lungs to be reduced. If this happens to such a degree that the patient cannot draw enough oxygen from his or her environment to maintain cellular respiration, then the victim may need supplemental oxygen.
  • Cavitary pneumonia is a process in which the alveoli are destroyed and produce a cavity. As the alveoli are destroyed, the surface area for gas exchange to occur becomes reduced. Further changes in blood flow can lead to decline in lung function.

References[edit]

  1. ^ Weibel, E. R. (1963). Academic Press, ed. Morphometry of the human lung. p. 151. ISBN 3-540-03073-5. 
  2. ^ Hansen, J. E.; Ampaya, E. P.; Bryant, G. H. and Navin, J. J. (1975). "The Branching Pattern of Airways and Air Spaces of a Single Human Terminal Bronchiole". Journal of Applied Physiology 38 (6): 983–989. PMID 1141138. 
  3. ^ Daniels, Christopher B. and Orgeig, Sandra (2003). "Pulmonary Surfactant: The Key to the Evolution of Air Breathing". News in Physiological Sciences 18 (4): 151–157. PMID 12869615. 
  4. ^ C. Michael Hogan. 2011. "Respiration". Encyclopedia of Earth. Eds. Mark McGinley & C. J. Cleveland. National council for Science and the Environment. Washington, D.C.
  5. ^ "Alveoli: Gas Exchange and Host Defense". Functional Ultrastructure: An Atlas of Tissue Biology and Pathology. Springer Vienna. 2005. pp. 224–225. doi:10.1007/b137527. ISBN 978-3-211-83564-7. 
  6. ^ "Clinical Naturopathic Medicine" Leah,Hechtman. pg.420. 2012
  7. ^ Roberts, M., Reiss, M., Monger, G. (2000) "Gaseous exchange". Advanced Biology. Surrey, Nelson. p. 167.
  8. ^ Ochs M., Nyengaard J. R., Jung A., Knudsen L., Voigt M., Wahlers T., Richter J., Gundersen H. J. G. (2004). "The number of alveoli in the human lung". American journal of respiratory and critical care medicine 169 (1): 120–4. doi:10.1164/rccm.200308-1107oc. PMID 14512270. 
  9. ^ Saladin, Kenneth S. (2007). Anatomy and Physiology: the unity of form and function. New York: McGraw Hill. ISBN 0-07-322804-4. 

External links[edit]

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