Architectonics and Cellular Composition of Alveoli
The respiratory system includes air-conducting pathways (from the nasal cavity to the terminal bronchioles) and the respiratory zone, where direct gas exchange occurs. Supportive roles are played by the rib cage, intercostal muscles, diaphragm, pleural cavities, as well as intrinsic neural and endocrine apparatuses. The vascular network is a crucial component at all stages.
Alveolar walls are formed by a simple squamous epithelium resting on a basement membrane. Its cellular composition includes:
- Type I alveolar cells (Type I pneumocytes): Large, flattened cells. They occupy 95% of the entire surface and serve as the main site of gas exchange.
- Type II alveolar cells (Type II pneumocytes): Cover the remaining 5% of the surface area. They do not directly participate in gas exchange.
- Neuroendocrine cells (Kulchitsky cells, or third-order 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 portion of the Type I pneumocyte (0.2 µm).
- Fused basement membrane (0.1 µm) — the site of tight adhesion between the epithelial and capillary membranes.
- Endothelial cell of the blood vessel (0.2 µm).
An important component of the barrier is also the surfactant film lining the internal 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 frequently associated with the impairment of these protective 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, epinephrine, and norepinephrine 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 take place here.
- Hemodynamics and thermoregulation: The lungs act 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 respiratory hypoxia. Acute oxygen deprivation triggers cor pulmonale and cardiopulmonary failure, while chronic hypoxia 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 (hydrostatic) pressure (8–10 mm Hg), which ensures reabsorption. Pulmonary edema develops if hydrodynamic pressure rises sharply (e.g., in acute heart failure) or if blood hypoonquia occurs.
Respiration also directly affects acid-base balance and potassium metabolism:
- Respiratory acidosis (in respiratory failure) leads to hyperkalemia.
- Respiratory alkalosis causes a drop in plasma potassium concentration (hypokalemia).