Architectonics and cellular composition of alveoli
The respiratory system includes the air-conduction pathways (from the nasal cavity to the bronchioles) and the respiratory division, where gas exchange directly takes place. Supporting roles are played by the chest cage, intercostal muscles, diaphragm, pleural cavities, as well as intrinsic neural and endocrine apparatuses. The vascular network is a crucial component at all stages.
The alveolar walls are formed by a single-layer epithelium resting on a basement membrane. Its cellular composition includes:
- Type I pneumocytes: large flattened cells. They occupy 95% of the total surface and serve as the main site of gas exchange.
- Type II pneumocytes: cover the remaining 5% of the area. They do not directly participate in gas exchange.
- Neuroendocrine cells (Kulchitsky cells, or tertiary pneumocytes): located among the alveolar epithelium, between basal cells in the bronchi, near nerve endings, and in the stroma close to blood vessels.
Air-blood barrier
This is the primary site of gas exchange in the body. The barrier is formed by capillaries and closely apposed type I pneumocytes.
The total thickness of this barrier is only 0.5 µm. It consists of three layers:
- Flattened part of a type I pneumocyte (0.2 µm).
- Shared basement membrane (0.1 µm) — the site where the epithelial and capillary membranes closely adhere.
- Blood vessel endothelial cell (0.2 µm).
An important component of the barrier is also the surfactant film lining the inner surface of the alveoli.
Non-respiratory functions
In addition to air conditioning (warming in the nasal passages and humidification), the lungs actively participate in metabolism and homeostasis maintenance. Organ diseases are often associated with impairments in these exact defense mechanisms.
- Metabolism: regulation of water-salt, protein, and carbohydrate balance. The organ is characterized by a high rate of lipid metabolism (biogenesis of surfactant, leukotrienes, prostaglandins).
- Inactivation of biologically active substances (BAS): serotonin, histamine, bradykinin, adrenaline, and noradrenaline are degraded in the lung tissue. The generation and inactivation of prostaglandins, reactive oxygen species (ROS), as well as the inactivation of angiotensin-converting enzyme (ACE), also occur here.
- Hemodynamics and thermoregulation: the lungs serve as a blood reservoir, regulate blood clotting, clear the bloodstream of microthrombi and metabolic products. The body loses 5–10% of its heat through exhaled air.
Pathophysiology and fluid balance
Pathological processes (tumors, inflammation, pulmonary sclerosis) lead to the development of respiratory hypoxia. Acute oxygen deprivation triggers cor pulmonale and heart failure, while chronic deprivation causes sclerotic, atrophic, and dystrophic changes both in the lung tissue itself and in internal organs (primarily affecting the cardiovascular system).
Lung tissue is capable of actively absorbing fluid from the alveoli. Normally, capillary oncotic pressure (25–30 mm Hg) significantly exceeds hydrodynamic pressure (8–10 mm Hg), ensuring reabsorption. Pulmonary edema develops if hydrodynamic pressure rises sharply (e.g., in acute heart failure) or if blood hypo-oncia occurs.
Respiration also directly affects acid-base balance and potassium metabolism:
- Respiratory acidosis (in respiratory failure) leads to hyperkalemia.
- Respiratory alkalosis causes a decrease in plasma potassium concentration (hypokalemia).
Briefly: answers to topical questions
What are the functions of type II pneumocytes?
Type II pneumocytes (type 2 alveolocytes) perform secretory and cambial functions while not directly participating in gas exchange.
- Secretory function — release of cytophospholiposome contents into the alveolar lumen to form surfactant (they act as the "surfactant factory").
- Cambial function — act as stem cells, ensuring the regeneration of the alveolar epithelium.
What pathomorphological changes occur in internal organs during chronic respiratory hypoxia?
In chronic respiratory hypoxia, dystrophic, atrophic, and sclerotic processes develop in internal organs. The cardiovascular system is the first to suffer. Such processes also develop within the lung tissue itself. Alterations in the gas composition of arterial blood and sclerotic changes demand strain on compensatory mechanisms, leading to morphological remodeling of the respiratory system sections.
Which cells synthesize surfactant in the lungs?
Surfactant in the lungs is synthesized by type 2 pneumocytes and non-bordered epitheliocytes of the respiratory bronchioles. Type 2 pneumocytes are also called secretory or large alveolocytes and serve as the "surfactant factory." They possess a well-developed synthetic apparatus and release the contents of specific osmiophilic organelles — cytophospholiposomes — into the alveolar lumen to form surfactant.
What is the chemical composition of surfactant?
The chemical composition of surfactant includes lipids and proteins.
- Lipids — constitute 90% of the mass, represented predominantly by phospholipids and cholesterol. The main component (40% of the mass) is dipalmitoylphosphatidylcholine, containing two molecules of saturated palmitic acid.
- Proteins — constitute 10% of the mass and are subdivided into 4 groups.
Which macrophages are present in lung tissue and what is their function?
Alveolar macrophages belonging to the mononuclear phagocyte system are present in lung tissue. Their main function is defensive, realized through phagocytosis (engulfment and destruction of pathogens, body cells, dust particles, and erythrocytes). In an activated state, they are capable of generating reactive oxygen species and proteases. In pathologies (e.g., usual interstitial pneumonia), a monocytoid type of macrophage appears, which loses phagocytic activity but enhances protein synthesis and contains high levels of fibronectin.
For quick memorization of the layers of the blood-air barrier, use the "PBE" rule: Pneumocyte (Type I), Basal lamina (shared), Endothelium of the capillary. Surfactant lies on top of this structure.
Class and exam questions
Which cells occupy most of the alveolar surface?
Type I pneumocytes. They are large, flat, cover about 95% of the alveolar area, and serve as the main site of gas exchange.
Why does pulmonary edema occur in acute heart failure?
Due to a sharp increase in intracapillary hydrodynamic pressure. Normally, it is lower than oncotic pressure, allowing tissue to absorb fluid, but in pathology, this balance is disrupted.
How does respiratory failure affect blood potassium levels?
It triggers the development of respiratory acidosis, which, in turn, leads to an elevation of plasma potassium ion concentration (hyperkalemia).
What else to study on this topic
- Surfactant biogenesis and its role in pulmonary lipid metabolism
- Mechanisms of inactivation of biologically active substances in lung tissue
- Pathogenesis of cor pulmonale in acute hypoxia
- Effect of chronic hypoxia on the cardiovascular system
- Neuroendocrine apparatus of the lungs and functions of Kulchitsky cells
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