lungs elastic organs used for breathing in vertebrate animals, excluding most fish, which use gills , and a few amphibian species that respire through the skin. The word is sometimes applied to the respiratory apparatus of lower animals.

The human lungs are paired organs, located on either side of the heart and occupying a large portion of the chest cavity from the collarbone to the diaphragm. Air enters the body through a series of passages, beginning with the nose or mouth. It travels to the chest cavity through the trachea , which divides into two bronchi, each of which enters a lung. The bronchi divide and subdivide into a network of countless tubules. The smallest tubules, or bronchioles, enter cup-shaped air sacs known as alveoli, which number about 700 million in both lungs. Each alveolus is surrounded by a net of capillaries. As blood flows through these vessels, carbon dioxide passes into the alveoli, and oxygen diffuses into the bloodstream. The capillaries are part of a vast network of pulmonary blood vessels that connect the lungs directly to the heart via the large pulmonary arteries and veins. The alveoli are clustered in groups, or lobules, and the lobules are clustered into lobes.

In humans, the left lung has two lobes; the right lung three. The lungs are covered by a thin membrane called the pleura . They are expanded and contracted (thereby inhaling and exhaling air) by the combined movement of the diaphragm and the rib cage, which is alternately raised (expansion) and lowered (contraction) by the chest muscles. In recent years, smoking has been found to cause severe and sometimes fatal diseases of the lung, such as cancer and emphysema. Pneumonia is an inflammation of the lung tissue caused by various agents or organisms such as viruses. Asthma, a hypersensitivity or allergic response to some stimuli, covers a range of severity and is characterized by bronchial spasms and difficult breathing. See respiration .

lungs Organs of the respiratory system of vertebrates, in which the exchange of gases between air and blood takes place. The lungs lie in the pleural cavity within the ribcage. Two sheets of tissue (the pleura) line this cavity: one coats the lungs, and the other lines the walls of the thorax. Between the pleura is a fluid that cushions the lungs and prevents friction. Light and spongy, lung tissue consists of tiny air sacs, called alveoli, which are served by networks of fine capillaries. See also alveolus; gas exchange; ventilation

lungs The name ‘lungs’ is derived from their lightness in weight, since they contain air, and the butcher refers to them as ‘lights’ for this reason. Adult lungs will float in water, but lungs from a fetus who has not breathed will sink. ‘Pulmonary’, from the Latin, refers to the lungs and is used in medical terminology, as in pulmonary function tests or pulmonary disease.

When the lungs are taken out of the chest they partially collapse. This is because they contain elastic fibres in the walls of the airways and alveoli (air sacs); open a festive balloon and it will empty itself. In addition, a thin layer of liquid lining the alveoli exerts surface tension, tending to collapse the lungs, although this surface tension is greatly decreased by the presence of surfactant. A soap bubble will collapse when pricked, although it has no elastic material; the surface tension of the film provides force enough.

The function of the lungs is to provide an enormous surface for gas exchange, with oxygen entering the body and carbon dioxide leaving it. The surface has to be protected against physical and environmental assault, in this respect resembling the internal gills of fishes and differing from the external gills of, for example, tadpoles. Thus the lungs are encased in structures — the chest wall and diaphragm — which will also provide the means of its ventilation. Amphibia inflate their lungs by pumping air in from the mouth; mammals, far more active and usually much larger, suck air into the lungs by muscular effort which creates a negative pressure around them.

Our knowledge of the structure and func-tion of the lungs has depended on two major technological advances over the past three centuries: the light microscope and, later, the electron microscope. For almost two thousand years it was thought that the lungs were generally similar in structure to the liver, spleen, and pancreas, the only important difference being that air could enter the lungs through the trachea to mix physically with blood, cooling it by passing into the blood vessels. The superb anatomical dissections of Leonardo da Vinci (1452–539) and Versalius (1514–64) were regarded as consistent with this view. It was the use of the microscope by Malpighi (1628–94) that demonstrated for the first time the air-filled alveoli, the blind ends of the air passages into the lungs. He described them as ‘an almost infinite number of orbicular bladders’. Malpighi also showed that the blood capillaries in the lungs were vessels with walls that separated blood from gas, and allowed the passage of blood through the lungs, as deduced but not demonstrated by William Harvey. However, Malpighi knew nothing of gas exchange and thought the function of alveolar ventilation (the flow of air in and out of the alveoli) was to stir and mix the blood in the capillaries. From the 1950s onwards, the electron microscope displayed in detail the structures of the walls of the alveoli and of the tracheobronchial tree, extending to ‘ultrastructure’ within cells, knowledge of which had advanced meanwhile as light microscopy improved.

The airways below the larynx consist of (i) the trachea, a tube that extends almost to the middle of the chest; (ii) the bronchi (bronchial tree), formed by the trachea splitting into two and then each branch dividing again; (iii) the bronchioles — thin and short distensible airways that again divide many times to form (iv) the alveolar ducts from which (v) the alveoli arise. This multiple division results in about 23–5 generations of airway, with geometrically increasing numbers and total cross-sectional areas, and decreasing diameters. For example, from one trachea with a diameter of about 180 mm in an adult, by the tenth generation we have 1000 bronchi, each with a diameter of about 1.3 mm; by the twentieth generation we have 1 million bronchioles, each with a diameter of about 0.5 mm; and right at the end there are about 300 million alveoli. The diameter of the alveoli, like that of the bronchi and bronchioles, varies with the degree of lung inflation, in the range 0.1–0.3 mm. The alveolar surface area may be 30–100 m² — often described as the size of a tennis court.

In the human embryo the lungs first begin to develop at about 3 weeks after fertilization. The alimentary tract develops earlier, and a ‘bud’ from its ventral surface progressively extends into the chest to form the airways and lungs. This common embryological source of the lungs and gut is reflected in adult structure and function; thus there are similarities in that both have smooth muscle in their walls, glandular secretion of mucus from their linings, and a nerve supply from the autonomic nervous system, although of course other differences in structure and function are considerable. At about 16 weeks alveoli begin to appear, looking rather like glands with thick walls. Only at about 20–25 weeks does the lung begin to resemble the adult tissue. Even at full-term birth the lungs, although functionally adequate, are not fully developed anatomically, having fewer bronchial branches and a far smaller alveolar surface area than they eventually acquire.

The airways: trachea, bronchi, and bronchioles

These are the conducting airways, and do not take part in gas exchange. Their function is to condition the air we breathe in and to conduct it to the alveoli. If inspired air reached the alveoli directly, if it were cold it would cool the tissue, if hot it would heat it, and if dry it would parch and destroy the alveolar walls. Only if we breathed air at 37°C and 100% humidity — a rare occurrence — would we avoid tissue damage. When we breathe through the mouth, as in exercise or with nasal blockage, we have eliminated the air conditioning role of the nose, and the mouth is much less efficient for this purpose. If the inspired air is cold and dry it will be raised to body temperature and full humidity by the first few generations of bronchi. This makes the airway lining itself (the mucosa) cold and dry, but protects the alveoli. On breathing out the mucosa will take up heat and water vapour from the expired air, restoring it to normal. Not only are the alveoli protected, but loss of heat and water from the body as a whole is minimized.

The walls of the trachea and bronchi have several layers. On the inner lining surface, the ‘luminal’ side, there is a layer of epithelium as a kind of skin. Most of the epithelial cells are ciliated, with microscopic ‘hairs’ (cilia) that continuously sweep any surface material towards the larynx, where it is coughed up or swallowed. This is the ‘ciliary escalator’. Other cells secrete mucus, the slimy liquid that constitutes phlegm and lies on the cilia. Just under the epithelium is a dense blood capillary network that provides nutrition for the epithelium and glands, and may be the site of uptake of inhaled pollutants and drugs. Deeper in the wall are the submucosal glands, the main source of the mucus that lines the airways. The glands are stimulated to secrete by many factors, the most important being pollutants, including cigarette smoke, and viral or bacterial infections of the airways. Smoker's cough brings up the mucus thus secreted, and in chronic bronchitis there is the overproduction of mucus that characterizes the disease and is due to local pathological changes. The secreted mucus normally has several important defensive effects. It will create a barrier and take up soluble pollutants and smoke particles, slowing down their entry into the body and protecting the epithelium from their harmful effects, and eliminating them via the ciliary escalator. It will stimulate cough as an even more rapid means of their removal. In health the mucus sheet is very thin and difficult to measure; it is probably about 0.02–0.05 mm thick. Even in disease when the output of mucus is greatly increased, it remains too thin to block the airways, unless there is associated inflammation.

Deeper in the airway wall there is cartilage and smooth muscle. The cartilage stabilizes the airways and prevents their collapse during vigorous acts of breathing, such as coughing. The smooth muscle has not been shown to have a physiological role, unlike that in the intestines, which is responsible for the squeezing movement of peristalsis, but possibly it adjusts the diameter of the airways to make them optimally efficient for conducting gas to the alveoli.

The trachea and bronchi contain many sensory nerves, in general of two types. In the smooth muscle are receptors that signal the degree of stretch and therefore of inflation of the airways and lungs, and control the pattern of breathing — its rate and depth, probably to make it as efficient as possible. If the vagus nerves that carry sensory information from the bronchi are cut, in most animals the breathing becomes slow, deep, and mechanically inefficient. Secondly, in the epithelium there is a network of fine nerve fibres, with finger-like projections reaching almost to the airway lumen, that respond to inhaled pollutants and inflammatory mediators and set up a range of reflex responses. The most striking is the cough, but there is also reflex mucus secretion and smooth muscle contraction. The nerves look like, and act as, tripwires and sensing rods just under the surface, ready to respond to any adverse intruder.

The smallest air-conducting vessels, the bronchioles, are distinguished by having no cartilage in their walls, no mucus cells in their epithelium, and few or no submucosal glands. When the lungs inflate they probably distend equally with the alveoli, but there is little gas exchange in them. If they are inflamed, as in bronchiolitis, the alveoli they supply collapse, with a stiffening of the lungs and a failure of gas exchange.

Because the airways take no part in gas exchange, they are sometimes referred to as the ‘anatomical deadspace’. At rest their volume is about 150 ml in a healthy adult. If an average tidal volume of 500 ml is inhaled, at the end of inspiration only 350 ml will have entered the alveoli, and 150 ml will remain in the airways. The ventilation used for gas exchange will be only 350/500ths — or 70% — of the total ventilation. The rest could be called wasted ventilation but, as described earlier, it has an essential function in conditioning the inspired air. When we breathe out, the first 150 ml is unchanged ‘fresh’ air, followed by 350 ml of air from the alveoli, rich in carbon dioxide and partly depleted of oxygen.

Asthma

In asthma the contraction of bronchial smooth muscle can have a profound effect by narrowing the airways; a greater muscular effort is then required to inflate the lungs. The smooth muscle contracts in response to two main stimuli, chemical and nervous, and either can cause the wheezing associated with asthma. Most types of asthma involve inflammation, with release of chemical mediators like histamine, bradykinin, and substance P, which diffuse to the smooth muscle and make it contract. In addition, nervous signals can come down from the brain via the vagus nerves, when asthma and wheezing are induced by emotional factors in susceptible subjects.

It used to be thought that asthma was solely due to smooth muscle contraction narrowing the airways. This view was supported by the effectiveness of treatment by smooth muscle relaxants such as salbutamol. But asthma is now considered to be an inflammation of the airways, with multiple effects that all narrow the airways: smooth muscle contraction, thickening of the mucosa by oedema because of leaking blood vessels, and secretion of mucus into the airway lumen. The use of anti-inflammatory drugs has become general.

The alveolar ducts and alveoli

Here gas exchange takes place. There are about 15 million alveolar ducts, and each gives rise to about 20 alveolar air sacs. Each of these alveoli is surrounded by a network of blood capillaries — a bit like a balloon in a close-fitting string bag except that the alveoli are not spherical, and they share the ‘string’ with the adjacent alveoli all around (see figure for shape in cross-section). The entire output of the right heart goes through the alveolar blood vessels and then into the left heart. The enormous alveolar surface, up to 300 m², promotes gas exchange between blood and air, since the rate of diffusion of a gas depends on the surface area, the thinness of the diffusion barrier, and the solubility of the gas (Fick's Law). The alveolar wall is extremely thin, from 0.2–0.5 μm, depending on the degree of inflation of the lungs. The barrier to diffusion has three components. On the surface of the alveoli is a thin layer of secretion, containing surfactant, the detergent phospholipid that lowers the surface tension of the lungs and allows them to be stretched by relatively low pressures. The surfactant layer is about 0.15 μm thick. Then there is the epithelial cell layer of the alveoli. This consists of two types of cells, those which mainly provide a mechanical sheet (type I) and those that secrete surfactant (type II). Together they constitute the lining ‘skin’ of the alveoli. The capillary endothelium is the third component of the barrier. Cells of a different type, the alveolar macrophages, are found within the cavities of the alveoli; their function is to ingest and remove solid particles, such as those of smoke.

Carbon dioxide is over twenty times more soluble than oxygen in body liquids, and diffuses twenty times more quickly out of the body than oxygen enters. In any diseases where alveolar gas exchange is decreased, for example when the alveolar wall is thickened by alveolitis, the first changes in blood gas transfer will be with oxygen, and the patient may develop quite severe hypoxia before the blood carbon dioxide begins to increase.

For many years at the beginning of the twentieth century there was intense scientific dispute as to whether the alveoli of the human lungs could secrete oxygen into the bloodstream. The argument was that at high altitudes the oxygen pressure was so low that it could not maintain blood oxygen pressure without active transport through the epithelium. Perhaps the indirect methods to test the problem were not sensitive enough for a clear solution — and it was known that some fishes could actively secrete oxygen into their swim bladders, taking advantage of the properties of their haemoglobin that did not seem to apply to human haemoglobin. The problem was finally solved when more sensitive analysis showed that human lungs, and presumably those of other mammals, could not secrete oxygen and that all gas exchanges could be explained by passive diffusion. Even in the absence of oxygen secretion, some climbers can just get to the top of Mount Everest without added oxygen.

John Widdicombe