All the gas exchange structures distal to a single terminal bronchiole represent an acinus. Thus, an acinus is a parenchymal lung unit in which all structures participate in gas exchange. The human lung fairly consistently has three generations of respiratory bronchioles that are followed by a number of divisions of alveolar ducts. Rats have from three to 13 divisions of alveolar ducts, and the human lung has a similar alveolar ductal architecture, with approximately nine generations of alveolar ducts.
A typical normal human lung contains approximately 30,000 to 40,000 terminal bronchioles and, by definition, the same number of acini. Each acinus is approximately 6 mm in diameter and has a volume of approximately 0.50 mm3. Acini vary substantially in size and typically contain 10,000 to 12,000 alveoli (Table 1).
TABLE 1. Structural characteristicsof the normal human lung
In older literature, divisions of the lung into primary and secondary lobules is described. The primary lobule refers to all respiratory tissue distal to a final respiratory bronchiole, and thus contains only alveolar ducts and alveolar sacs. Some animal species, such as the rat, have only rudimentary respiratory bronchioles, and in this situation a primary lobule is a useful concept to define aspects of ventilation and gas distribution in specific lung units. In the human, the primary lobule is not a very useful concept, because the acinus divides into multiple respiratory bronchioles and a high degree of collateral ventilation occurs between these subunits. Secondary lobules are lung units delineated by connective tissue septa; they are about 1 cm3 in size. They form structures that are clearly visible on the pleural or cut surface of the lung. The secondary lobule is supplied by a bronchiole with a diameter of about 1 mm that divides into five to 12 terminal bronchioles, and thus into a similar number of acini.
Alveoli
The gas exchange region of the lung is made up of approximately 500,000,000 alveoli having a total surface area of approximately 100 m2. These alveoli are highly vascularized, with the alveolar septal capillary bed having a vascular surface area of approximately 70 m2. The normal alveolar septa are approximately 10 µm thick. The alveolar air-capillary barrier is made up of variable thin and thick segments. The thin segment is composed of an alveolar epithelium, a fused epithelial and endothelial basement membrane, and a capillary endothelium. Because both type I epithelial cells and capillary endothelial cells are highly attenuated, the combined thickness of this air-blood barrier can be as little as 0.5 µm. The alveolar walls contain connective tissue, primarily collagen, which weaves through the capillary mesh. This and other cellular and acellular components of the interstitium create the thicker portions of the alveolar septal walls. Three-dimensional reconstructions of alveolar septal walls from rats have demonstrated that the alveolar entrance rings are particularly rich in both collagen and elastin. Alveolar mouths form the boundary of alveolar ducts (Fig. 10), and their entrance rings are linked together into a connective tissue structure that spirals down alveolar ducts, providing a connection between the openings or mouths of individual alveoli. Elastic tissue is most prominent along the alveolar duct openings. Collagen strands or fibers interlace across the alveolar walls and connect adjacent alveoli along a single alveolar duct as well as connect alveoli between two adjacent alveolar ducts.
FIG. 10. Scanning electron micrograph of the alveolar duct region from a rat lung. The alveolar duct walls are made up of alveolar mouth openings surrounded by flattened alveolar septal edges forming the entrance rings around the alveolar openings. The primary collagen and elastin network lining the alveolar ducts is under tension in this fully expanded lung.
Based on morphologic evidence of collagen and elastin distributions and the effects of surfactant depletion on the structure of alveoli and alveolar ducts, Wilson and Bachofen developed a model of lung micromechanics comparing the contributions of alveoli and alveolar ducts to lung elasticity. This model suggests that elastic components abundant in the walls of alveolar ducts are primarily responsible for the function of alveolar ducts, whereas surface tension effects are primarily responsible for the tension in alveoli. Three-dimensional reconstructions of alveoli and alveolar ducts as transpulmonary pressure is raised from 0 to 30 cm H2O demonstrate that at low lung volumes alveoli make up 80% of the parenchymal lung volume and dominate the gas volume changes. As pulmonary pressure increases, the contributions to changes in volume by both alveoli and alveolar ducts converge (Fig. 11). This suggests that at high lung volumes connective tissue elements, both between and within the alveolar ducts, come under tension and act to equalize further changes in volume between alveoli and alveolar ducts. This both limits overextension of alveoli and enhances lung stability by distributing stress among all contributing units of an alveolar duct interconnected by elastic and collagenous structures.
FIG. 11. Volume ratios of alveoli and alveolar ducts as a function of the transpulmonary extending pressure. These pressure-volume relationships were determined using morphometric point-counting procedures to estimate the relative contributions of alveoli and alveolar ducts during lung expansion. At low lung volumes, alveoli make up the majority (80%) of the lung parenchyma. As lung volume increases, alveolar ducts initially show the greatest change in volume, and they increase from 20% to almost 50% of the volume of the lung parenchyma. At about 10 cm of water pressure, the two curves converge, showing that changes in volume of these two compartments are proportionally similar from intermediate to high lung volumes or pressures. The convergence of these two curves at higher pressures suggests that the connective tissue elements within and between the alveolar ducts are under tension and help stabilize the lung by equally distributing further increases in lung volume.
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