The alveoli are the tiny air sacs in the lungs where gas exchange happens. And their walls are lined by a thin film of water, which creates a force at their surface called surface tension.
Surface tension tends to collapse the pulmonary alveoli, and, as you can imagine, this could turn into a big problem - not being able to breathe in.
Luckily, alveolar cells have found a way to counteract surface tension by producing surfactant, which is a phospholipoprotein that reduces the surface tension, keeping the alveoli open so that we can breathe properly.
That being said, take a deep breath, because we’re about to delve into the physics of surface tension.
The water molecules, known as H2O to their friends, stay close together because of hydrogen bonds that form between the negatively charged oxygen ion of one molecule and the positively charged hydrogen ion of another molecule.
Within the bulk of water, the molecules are equally pulled in every direction by neighboring molecules, so the resulting net force is zero.
However, when you add air into the mix, the whole system becomes unbalanced, because at the water-air interface, water molecules are not surrounded by other water molecules.
This creates too many cohesive forces between water molecules at the surface, that pull the water molecules at the surface closer together, making the surface of the water shrink to the minimum surface area possible.
Now, the interior of the alveoli is also spherical, so the net force of surface tension is directed to the center of the alveoli, which tends to collapse the alveolar walls towards the center.
The magnitude of this force is predicted by Laplace law, which states that the pressure collapsing the alveolus is directly proportional to the surface tension generated by molecules of fluid lining the alveolus, and inversely proportional to the radius of the alveoli. So the smaller the alveoli, the larger the collapsing pressure.
Now, when we breathe out, alveolar size decreases, because the air that was inflating it is now expelled from the lungs.
This means that the alveolar radius reduces, which increases the collapsing pressure according to Laplace.
It also means that for inspiration to occur – which is literally trying to inflate the alveoli, it will take too much force to first overcome this collapsing pressure, meaning the entire inspiration process will be quite difficult.
Difficulty in inflating individual lung alveoli results in reduced lung compliance, which is the ability of the lung to stretch and inflate as a whole.
Luckily enough, this doesn’t happen in normal individuals, because human alveoli synthesize a lipoprotein compound called pulmonary surfactant.
The surfactant lines the alveolar walls over the water film, and then reduces the surface tension and thus the collapsing pressure.
Diving deep into this, let’s zoom in and look at a cross-section of the wall of the pulmonary alveoli. It largely consists of type I pneumocytes, which are flat squamous epithelial cells.
These cells are very thin and widespread making up to 97 % of the whole alveolar surface, which ensures an efficient diffusion needed in gas exchange between the alveoli and blood within a surrounding capillary network.
Next to type I pneumocytes lies type II pneumocytes, which are cuboidal cells that contain lamellar bodies - the organelles that secrete pulmonary surfactant.
In humans, lamellar bodies start producing surfactant at 24 to 28 weeks of gestational age, and usually by the week of 35, alveoli have enough surfactant to keep them from collapsing.
Now, let's have a look at the pulmonary surfactant itself. It is a phospholipoprotein complex, consisting mainly of Dipalmitoyl phosphatidylcholine or just DPPC, and some proteins such as surfactant proteins – A and D.