High-Resolution CT of the Lung
3rd Edition

Chapter 2
Normal Lung Anatomy
The accurate interpretation of high-resolution computed tomography (HRCT) images requires a detailed understanding of normal lung anatomy and of the pathologic alterations in normal lung anatomy occurring in the presence of disease [1,2,3,4]. In this chapter, only those aspects of lung anatomy that are important in using and interpreting HRCT are reviewed.
Lung Interstitium
The lung is supported by a network of connective tissue fibers called the lung interstitium. Although the lung interstitium is not generally visible on HRCT in normal patients, interstitial thickening is often recognizable. For the purpose of interpretation of HRCT and identification of abnormal findings, the interstitium can be thought of as having several components (Fig. 2-1) [5].
The peribronchovascular interstitium is a system of fibers that invests bronchi and pulmonary arteries (Fig. 2-1). In the perihilar regions, the peribronchovascular interstitium forms a strong connective tissue sheath that surrounds large bronchi and arteries [6]. The more peripheral continuum of this interstitial fiber system, which is associated with small centrilobular bronchioles and arteries, may be termed the centrilobular interstitium (Fig. 2-1). Taken together, the peribronchovascular interstitium and centrilobular interstitium correspond to the “axial fiber system” described by Weibel, which extends peripherally from the pulmonary hila to the level of the alveolar ducts and sacs [5].
The subpleural interstitium is located beneath the visceral pleura; it envelops the lung in a fibrous sac from which connective tissue septa penetrate into the lung parenchyma (Fig. 2-1). These septa include the interlobular septa, which are described in detail below. The subpleural interstitium and interlobular septa are parts of the “peripheral fiber system” described by Weibel [5].
The intralobular interstitium is a network of thin fibers that forms a fine connective tissue mesh in the walls of alveoli and thus bridges the gap between the centrilobular interstitium in the center of lobules and the interlobular septa and subpleural interstitium in the lobular periphery (Fig. 2-1). Together, the intralobular interstitium, peribronchovascular interstitium, centrilobular interstitium, subpleural interstitium, and interlobular septa form a continuous fiber skeleton for the lung (Fig. 2-1). The intralobular interstitium corresponds to the “septal fibers” described by Weibel [5].
Large Bronchi and Arteries
Within the lung parenchyma, the bronchi and pulmonary artery branches are closely associated and branch in parallel. As indicated in the previous section, they are encased by the peribronchovascular interstitium, which extends from the pulmonary hila into the peripheral lung. Because some lung diseases produce thickening of the peribronchovascular interstitium in the central or perihilar lung, in relation to large bronchi and pulmonary vessels it is important to be aware of the normal HRCT appearances of the perihilar bronchi and pulmonary vessels.
When imaged at an angle to their longitudinal axis, central pulmonary arteries normally appear as rounded or elliptic opacities on HRCT, accompanied by uniformly thin-walled bronchi of similar shape (Fig. 2-2). When imaged along their axis, bronchi and vessels should appear roughly cylindrical or show slight tapering as they branch, depending on the length of the segment that is visible; tapering of a vessel or bronchus is most easily seen when a long segment is visible.
FIG. 2-1. Components of the lung interstitium. Taken together, the peribronchovascular interstitium and centrilobular interstitium correspond to the “axial fiber system” described by Weibel [5]. The subpleural interstitium and interlobular septa correspond to Weibel’s “peripheral fiber system.” The intralobular interstitium is roughly equivalent to the “septal fibers” described by Weibel.
FIG. 2-2. Normal appearances of large bronchi and arteries photographed with window settings of -600/2,000 HU (A) and -700/1,000 HU (B). The diameters of vessels and their neighboring bronchi are approximately equal. The outer walls of bronchi and pulmonary vessels are smooth and sharply defined. Bronchi are usually invisible within the peripheral 2 cm of lung, despite the fact that vessels are well seen in this region.
TABLE 2-1. Relation of airway diameter to wall thickness
Airway Diameter
Wall thickness
Lobular and segmental bronchi 5-8 1.5
Subsegmental bronchi/bronchiole 1.5-3.0 0.2-0.3
Lobular bronchiole 1 0.15
Terminal bronchiole 0.7 0.1
Acinar bronchiole 0.5 0.05
   Modified from Weibel ER. High resolution computed tomography of the pulmonary parenchyma: anatomical background. Presented at: Fleischner Society Symposium on Chest Disease; 1990; Scottsdale, AZ.


The diameter of an artery and its neighboring bronchus should be approximately equal, although vessels may appear slightly larger than their accompanying bronchi, particularly in dependent lung regions. Although the presence of bronchi larger than their adjacent arteries is often assumed to indicate bronchial dilatation, or bronchiectasis, bronchi may appear larger than adjacent arteries in a significant number of normal subjects. In an HRCT study of normal subjects, Lynch et al. [7] compared the internal diameters of lobular, segmental, subsegmental, and smaller bronchi to those of adjacent artery branches. Nineteen percent of bronchi had an internal bronchial diameter longer than the artery diameter, and 59% of normal subjects showed at least one such bronchus. Furthermore, a bronchus may appear larger than the adjacent artery branches if the scan traverses an undivided bronchus near its branch point, and its accompanying artery has already branched. In this situation, two artery branches may be seen to lie adjacent to the “dilated” bronchus.
FIG. 2-3. Normal appearances of large bronchi and arteries. In an isolated lung, the smallest bronchi visible (arrows) measures 2 to 3 mm in diameter. Bronchi and bronchioles are not visible within the peripheral 1 cm of lung, although the artery branches that accompany these bronchi are sharply seen. (Note: The “isolated” lungs illustrated in this volume are fresh lungs obtained at autopsy and scanned while inflated with air at a pressure of approximately 30 cm of water [10].)
The outer walls of visible pulmonary artery branches form a smooth and sharply defined interface with the surrounding lung, whether they are seen in cross section or along their length. The walls of large bronchi, outlined by lung on one side and air in the bronchial lumen on the other, should appear smooth and of uniform thickness. Thickening of the peribronchial and perivascular interstitiums can result in irregularity of the interface between arteries and bronchi and the adjacent lung [4,6,8].
Assessment of bronchial wall thickness on HRCT is quite subjective and is dependent on the window settings used [7]. Also, because the apparent thickness of the bronchial wall represents not only the wall itself, but the surrounding peribronchovascular interstitium as well, peribronchovascular interstitial thickening can result in apparent bronchial wall thickening (so-called peribronchial cuffing) on HRCT.
The wall thickness of conducting bronchi and bronchioles is approximately proportional to their diameter, at least for bronchi distal to the segmental level. In general, the thickness of the wall of a bronchus or bronchiole less than 5 mm in diameter should measure from one-sixth to one-tenth of its diameter (Table 2-1) [9]; however, precise measurement of the wall thickness of small bronchi or bronchioles is difficult, as wall thickness approximates pixel size.
Because bronchi taper and become thinner-walled as they branch, they become more difficult to see as they become more peripheral. Bronchi less than 2 mm in diameter are not normally visible on HRCT, and bronchioles within 2 cm of the pleural surface tend to be inconspicuous (Figs. 2-2 and 2-3) [10,11]. It is rare for normal bronchioles to be visible within 1 cm of the pleural surface [12,13].
Secondary Pulmonary Lobule
The secondary pulmonary lobule as defined by Miller refers to the smallest unit of lung structure marginated by connective tissue septa [9,14]. Secondary lobules are easily visible on the surface of the lung because of these septa (Fig. 2-4) [9,15]. The terms secondary pulmonary lobule, secondary lobule, and pulmonary lobule are often used interchangeably, and are used as synonyms in this book. The term primary pulmonary lobule has also been used by Miller to describe a much smaller lung unit associated with a single alveolar duct [16,17], but this designation is not in common use.
Secondary pulmonary lobules are irregularly polyhedral in shape and somewhat variable in size, measuring approximately

1 to 2.5 cm in diameter in most locations (Fig. 2-5) [5,9,15,18,19]. In one study, the average diameter of pulmonary lobules measured in several adults ranged from 11 to 17 mm [19]. Each secondary lobule is supplied by a small bronchiole and pulmonary artery, and is variably marginated, in different lung regions, by connective tissue interlobular septa containing pulmonary vein and lymphatic branches [16].
FIG. 2-4. Pulmonary lobular anatomy. A: Pulmonary lobules that are irregularly polyhedral or conical in shape are often visible on the surface of the lung, as shown in this diagram of five lobules visible on the posterior surface of the left lung. B: Lobules are supplied by small bronchiolar and pulmonary artery branches, which are central in location, and are variably marginated by connective tissue interlobular septa that contain pulmonary vein and lymphatic branches.
Secondary pulmonary lobules are made up of a limited number of pulmonary acini, usually a dozen or fewer, although the reported number varies considerably in different studies (Fig. 2-5A) [20,21]; in a study by Nishimura and Itoh [22], the number of acini counted in lobules of varying sizes ranged from three to 24. A pulmonary acinus is defined as the portion of the lung parenchyma distal to a terminal bronchiole and supplied by a first-order respiratory bronchiole or bronchioles [23]. Because respiratory bronchioles are the largest airways that have alveoli in their walls, an acinus is the largest lung unit in which all airways participate in gas exchange. Acini are usually described as ranging from 6 to 10 mm in diameter [19,24].
As indicated at the beginning of this section, Miller has defined the secondary lobule as the smallest lung unit marginated by connective tissue septa. Reid has suggested an alternate definition of the secondary pulmonary lobule, based on the branching pattern of peripheral bronchioles, rather than the presence and location of connective tissue septa (Fig. 2-6) [16,21,23]. On bronchograms, small bronchioles can be seen to arise at intervals of 5 to 10 mm from larger airways

(the so-called centimeter pattern of branching); these small bronchioles then show branching at approximately 2-mm intervals (the “millimeter pattern”) [23]. Airways showing the millimeter pattern of branching are considered by Reid to be intralobular, with each branch corresponding to a terminal bronchiole [21]. Lobules are considered to be the lung units supplied by 3 to 5 “millimeter pattern” bronchioles. Although Reid’s criteria delineate lung units of approximately equal size, about 1 cm in diameter and containing 3 to 5 acini, it should be noted that this definition does not necessarily describe lung units equivalent to secondary lobules as defined by Miller and marginated by interlobular septa (Fig. 2-6) [21,22], although a small Miller’s lobule can be the same as a Reid’s lobule. Miller’s definition is most applicable to the interpretation of HRCT and is widely accepted by pathologists, because interlobular septa are visible on histologic sections [22]. In this book, we use the term secondary pulmonary lobule to refer to a lobule as defined by Miller.
FIG. 2-5. A: Anatomy of the secondary pulmonary lobule, as defined by Miller. Two adjacent lobules are shown in this diagram. B: Radiographic anatomy of the secondary pulmonary lobule. Radiograph of a 1-mm lung slice taken from the lower lobe. Two well-defined secondary pulmonary lobules are visible. Lobules are marginated by thin interlobular septa (S) containing pulmonary vein (V) branches. Bronchioles (B) and pulmonary arteries (A) are centrilobular. Bar = 1 cm. (Reprinted from Itoh H, Murata K, et al. Diffuse lung disease: pathologic basis for the high-resolution computed tomography findings. J Thorac Imaging 1993;8:176, with permission.)
FIG. 2-6. Relative size and relationships of “Miller’s lobule” and “Reid’s lobule.”

Anatomy of the Secondary Lobule and Its Components
An understanding of secondary lobular anatomy and the appearances of lobular structures is key to the interpretation of HRCT. HRCT can show many features of the secondary pulmonary lobule in normal and abnormal lungs, and many lung diseases, particularly interstitial diseases, produce characteristic changes in lobular structures [3,4,8,10,11,25,26]. Heitzman has been instrumental in emphasizing the importance of the secondary pulmonary lobule in the radiologic diagnosis of lung disease [15,16,27].
As discussed in Chapter 1, the visibility of normal lobular structures on HRCT is related to their size and orientation relative to the plane of scan, although size is most important (Fig. 2-7). Generally, the smallest structures visible on HRCT range from 0.3 to 0.5 mm in thickness; thinner structures, measuring 0.1 to 0.2 mm, are occasionally seen.
For the purposes of the interpretation of HRCT, the secondary lobule is most appropriately conceptualized as having three principal parts or components:
  • Interlobular septa and contiguous subpleural interstitium
  • Centrilobular structures
  • Lobular parenchyma and acini
Interlobular Septa
Anatomically, secondary lobules are marginated by connective tissue interlobular septa, which extend inward from the pleural surface (Figs. 2-4 and 2-5). These septa are part of the peripheral interstitial fiber system described by Weibel (Fig. 2-1) [5], which extends over the surface of the lung beneath the visceral pleura. Pulmonary veins and lymphatics lie within the connective tissue interlobular septa that marginate the lobule.
It should be emphasized that not all interlobular septa are equally well defined. The interlobular septa are thickest and most numerous in the apical, anterior, and lateral aspects of the upper lobes, the anterior and lateral aspects of the middle lobe and lingula, the anterior and diaphragmatic surfaces of the lower lobes, and along the mediastinal pleural surfaces [28]; thus, secondary lobules are best defined in these regions. Septa measure approximately 100 μm (0.1 mm) in thickness in a subpleural location [3,5,10,11]. Within the central lung, interlobular septa are thinner and less well defined than peripherally, and lobules are more difficult to identify in this location.
Peripherally, interlobular septa measuring 100 μm or 0.1 mm in thickness are at the lower limit of HRCT resolution [11], but nonetheless they are often visible on HRCT scans performed in vitro [10]. On in vitro HRCT, interlobular septa are often visible as very thin, straight lines of uniform thickness that are usually 1 to 2.5 cm in length and perpendicular to the pleural surface (Figs. 2-7 and 2-8). Several septa in continuity can be seen as a linear opacity measuring up to 4 cm in length (Fig. 2-9) [10].
On clinical scans in normal patients, interlobular septa are less commonly seen and are seen less well than they are in studies of isolated lungs. A few septa are often visible in the lung periphery in normal subjects, but they tend to be inconspicuous (Fig. 2-10); normal septa are most often seen anteriorly and along the mediastinal pleural surfaces [4,29]. When visible, they are usually seen extending to the pleural surface. In the central lung, septa are thinner than they are peripherally and are infrequently seen in normal subjects (Fig. 2-9); often, interlobular septa that are clearly defined in this region are abnormally thickened. Occasionally, when interlobular septa are not clearly

visible, their locations can be inferred by locating septal pulmonary vein branches, approximately 0.5 mm in diameter. Veins can sometimes be seen as linear (Fig. 2-10B), arcuate, or branching structures (Fig. 2-10C-E), or as a row or chain of dots surrounding centrilobular arteries and approximately 5 to 10 mm from them. Pulmonary veins may also be identified by their pattern of branching; it is common for small veins to arise at nearly right angles to a much larger main branch.
FIG. 2-7. Dimensions of secondary lobular structures (A) and their visibility on HRCT (B).
Centrilobular Region and Centrilobular Structures
The central portion of the lobule, referred to as the centrilobular region or lobular core [16], contains the pulmonary artery and bronchiolar branches that supply the lobule, as well as some supporting connective tissue (the centrilobular interstitium described previously) [3,5,9,10,11]. It is difficult to precisely define lobules in relation to the bronchial or arterial trees; lobules do not arise at a specific branching generation or from a specific type of bronchiole or artery [9].
Branching of the lobular bronchiole and artery is irregularly dichotomous [22]. When they divide, they generally divide into two branches. Most often, they divide into two branches of different sizes, (one branch being nearly the same size as the one it arose from, and the other being smaller) (Fig. 2-5B). Thus, on bronchograms, arteriograms, or HRCT, there often appears to be a single dominant bronchiole or artery in the center of the lobule, which gives off smaller branches at intervals along its length.
The HRCT appearances and visibility of centrilobular structures are determined primarily by their size (Fig. 2-7). Secondary

lobules are supplied by arteries and bronchioles measuring approximately 1 mm in diameter, whereas intralobular terminal bronchioles and arteries measure approximately 0.7 mm in diameter, and acinar bronchioles and arteries range from 0.3 to 0.5 mm in diameter. Arteries of this size can be easily resolved using the HRCT technique [10,11].
FIG. 2-8. Interlobular septa in an isolated lung. Some thin, normal interlobular septa (small arrows) are faintly visible in the peripheral lung. Interlobular septa along the mediastinal pleural surface (large arrows) are slightly thickened by edema fluid and are more easily seen. Note that a very thin line is visible at the pleural surfaces and in the lung fissure, similar in appearance and thickness to the normal interlobular septa. This line represents the subpleural interstitial compartment and visceral pleura. (From Webb WR, Stein MG, et al. Normal and diseased isolated lungs: high-resolution CT. Radiology 1988;166:81, with permission.)
On clinical scans, a linear, branching, or dotlike opacity frequently seen within the center of a lobule, or within a centimeter of the pleural surface, represents the intralobular artery branch or its divisions (Figs. 2-10C-E, 2-11, and 2-12) [3,10,11]. The smallest arteries resolved extend to within 3 to 5 mm of the pleural surface or lobular margin and are as small as 0.2 mm in diameter [3,10,11]. The visible centrilobular arteries are not seen to extend to the pleural surface in the absence of atelectasis (Fig. 2-13).
Regarding the visibility of bronchioles in the lungs of normal patients, it is necessary to consider bronchiolar wall thickness rather than bronchiolar diameter. For a 1-mm bronchiole supplying a secondary lobule, the thickness of its wall measures approximately 0.15 mm; this is at the lower limit of HRCT resolution. The wall of a terminal bronchiole measures only 0.1 mm in thickness, and that of an acinar bronchiole only 0.05 mm, both of which are below the resolution of HRCT technique for a tubular structure (Fig. 2-7). In one in vitro study, only bronchioles having a diameter of 2 mm or more or having a wall thickness of more than 100

μm (0.1 mm) were visible using HRCT [11]; and resolution is certainly less than this on clinical scans. It is important to remember that on clinical HRCT, intralobular bronchioles are not normally visible, and bronchi or bronchioles are rarely seen within 1 cm of the pleural surface (Figs. 2-11 and 2-12) [12,13].
FIG. 2-9. lnterlobular septa in continuity in an isolated lung. On HRCT, long interlobular septa (arrows) can be seen marginating several secondary lobules. The septa in this lung are slightly thickened by fluid. Septa are well seen peripherally, but note that the septa and, therefore, secondary lobules are less well defined in the central lung. (From Webb WR, Stein MG, et al. Normal and diseased isolated lungs: high-resolution CT. Radiology 1988;166:81, with permission.)
Lobular (Lung) Parenchyma
The substance of the secondary lobule, surrounding the lobular core and contained within the interlobular septa, consists of functioning lung parenchyma–namely, alveoli and the associated pulmonary capillary bed–supplied by small airways and branches of the pulmonary arteries and veins. This parenchyma is supported by a connective tissue stroma, a fine network of very thin fibers within the alveolar septa called the intralobular interstitium (Fig. 2-1) [5,9], which is normally invisible. On HRCT, the lobular parenchyma should be of greater opacity than air (Fig. 2-14), but this difference may vary with window settings (see Chapter 1). Some small intralobular vascular branches are often visible.
It should be emphasized that all three interstitial fiber systems described by Weibel (axial, peripheral, and septal) are represented at the level of the pulmonary lobule (Fig. 2-1), and abnormalities in any can produce recognizable lobular abnormalities on HRCT [10]. Axial (centrilobular) fibers surround the artery and bronchiole in the lobular core, peripheral fibers making up the interlobular septa marginate the lobule, and septal fibers (the intralobular interstitium) extend throughout the substance of the lobule in relation to the alveolar walls.
FIG. 2-10. Normal HRCT in different subjects. A: HRCT in a normal subject; window mean/width: 600/2,000 HU. Interlobular septa are inconspicuous, and those few that are visible are very thin. The major fissures appear as thin, sharply defined lines. B: Two pulmonary vein branches (arrows) marginate a pulmonary lobule in the anterior lung, but the interlobular septa surrounding this lobule are very thin and difficult to see. The centrilobular artery lies equidistant between the veins. C: HRCT in a normal subject (-700/1,000 HU) shows few interlobular septa. A venous arcade (arrow) is visible in the lower lobe, with the centrilobular artery visible as a dot centered in the arcade. D: HRCT through the upper lobes in a normal subject (-700/1,000 HU). Normal interlobular septa (black arrows) are visible. The centrilobular artery (white arrow) is centered between them. E: In the same patient as D, a scan through the lower lobes shows normal pulmonary vein branches (black arrows) marginating pulmonary lobules. The centrilobular artery branches (white arrow) are visible as a rounded dot between the veins.
FIG. 2-11. Centrilobular anatomy in an isolated lung. A: On a CT scan obtained with 1-cm collimation, pulmonary artery branches (arrows) with their accompanying bronchi can be identified. B: On an HRCT scan at the same level, interlobular septa can be seen marginating one or more lobules (Fig. 2-9). Pulmonary artery branches (arrows) can be seen extending into the centers of pulmonary lobules, but intralobular bronchioles are not visible. The last visible branching point of pulmonary arteries is approximately 1 cm from the pleural surface. Bronchi are invisible within 2 or 3 cm of the pleural surface. (From Webb WR, Stein MG, et al. Normal and diseased isolated lungs: high-resolution CT. Radiology 1988;166:81, with permission.)
FIG. 2-12. Centrilobular anatomy in an isolated lung. Lobular core anatomy in an isolated lung. Branching pulmonary arteries (arrows) are visible within 1 cm of the pleural surface, but intralobular bronchioles are invisible. In the central lung, centrilobular arteries appear dotlike or as a branching structure. (From Webb WR, Stein MG, et al. Normal and diseased isolated lungs: high-resolution CT. Radiology 1988;166:81, with permission.)


Pulmonary Acinus
Pulmonary acini are not normally visible on HRCT [22]. As with lobules, acini vary in size. They are usually described as ranging from 6 to 10 mm in diameter and have been measured as averaging 7 to 8 mm in diameter in adults [19,24]. As indicated above, secondary pulmonary lobules defined by the presence of connective tissue interlobular septa usually consist of a dozen or fewer pulmonary acini (Fig. 2-5A) [9,19,20,24].
First-order respiratory bronchioles and the acinar artery branch measure approximately 0.5 mm in diameter (Fig. 2-7A); thus, intralobular acinar arteries are large enough to be seen on HRCT in some normal subjects [5,9,19,24]. Murata [11] has shown that pulmonary artery branches as small as 0.2 mm, associated with a respiratory bronchiole and thus acinar in nature, are visible on HRCT and extend to within 3 to 5 mm of the lobular margins or pleural surface (Fig. 2-7).
Lobular Anatomy and the Concept of Cortical and Medullary Lung
At least partially based on differences in lobular anatomy, it has been suggested that the lung can be divided into a peripheral cortex and a central medulla [16,30]. Although these terms are not in general use, the concept of cortical and medullary lung regions is useful in highlighting differences in lung anatomy and the varying appearances of secondary pulmonary lobules in the peripheral and central lung regions [31]. It also serves to emphasize some anatomic (and perhaps physiologic) differences between the peripheral and central lung that are useful in predicting the HRCT distribution of some lung diseases [32].
Peripheral or Cortical Lung
Cortical lung can be conceived of as consisting of two or three rows or tiers of well-organized and well-defined secondary pulmonary lobules, which together form a layer 3 to 4 cm in thickness at the lung periphery and along the lung surfaces adjacent to fissures (Fig. 2-15) [16,30]. The pulmonary lobules in the lung cortex are relatively large in size and are marginated by interlobular septa that are thicker and better defined than in other parts of the lung; thus, cortical lobules tend to be better defined than those in the central or medullary lung. Bronchi and pulmonary vessels in the lung cortex are relatively small; although cortical arteries and veins are visible on HRCT, bronchi and bronchioles are uncommonly visible. This contrasts with the anatomy of medullary lung, in which large vessels and bronchi are visible.
Lobules in the lung cortex tend to be relatively uniform in appearance and can be conceived of as being similar to the stones in a Roman arch: all of similar size and shape (Fig. 2-15) [30]. They can appear cuboid or be shaped like a truncated cone or pyramid [16]. However, it should be remembered that the size, shape, and appearance of pulmonary lobules as seen on HRCT are significantly affected by the orientation of the scan plane relative to the central and longitudinal axes of the lobules. A single scan typically traverses different parts of adjacent lobules (Figs. 2-8 and 2-9), resulting in widely varying appearances of the lobules, despite the fact that they are all of similar size and shape.
Central or Medullary Lung
Pulmonary lobules in the central or medullary lung are smaller and more irregular in shape than in the cortical lung and are marginated by interlobular septa that are thinner and less well defined. When visible, medullary lobules may appear hexagonal or polygonal in shape, but well-defined lobules are uncommonly seen in normals. In contrast with the peripheral lung, perihilar vessels and bronchi in the lung medulla are large and easily seen on HRCT.
FIG. 2-13. Normal lobular anatomy. HRCT (-700/1,000 HU) at two levels (A, B) in a normal subject shows artery branches extending to within 1 cm of the pleural surface. The arteries do not reach the pleura.
FIG. 2-14. Normal appearance of the lobular parenchyma. The lung parenchyma should appear to be homogeneously denser than air in the bronchi or, as in this isolated lung, denser than room air surrounding the specimen. The relative opacities of lung and air depend on the window settings.
FIG. 2-15. Corticomedullary differentiation in the lung. The lung cortex is composed of one or two rows or tiers of well-organized and well-defined secondary pulmonary lobules 3 to 4 cm in thickness. The pulmonary lobules in the lung cortex tend to be well defined and relatively large, and can be conceived of as being similar to the stones in a Roman arch: all of similar size and shape. The cortical airways and vessels are small, usually less than 2 to 3 mm in diameter.


Subpleural Interstitium and Pleural Surfaces
Diffuse infiltrative lung diseases involving the subpleural interstitium or pleura can result in abnormalities visible at the pleural surfaces.
Subpleural Interstitium and Visceral Pleura
The visceral pleura consists of a single layer of flattened mesothelial cells that is subtended by layers of fibroelastic connective tissue; it measures 0.1 to 0.2 mm in thickness [33,34]. The connective tissue component of the visceral pleura is generally referred to on HRCT as the subpleural interstitium, and is part of the “peripheral” interstitial fiber network described by Weibel (Fig. 2-1) [5]. The subpleural interstitium contains small vessels, which are involved in the formation of pleural fluid, and lymphatic branches. Interstitial lung diseases that affect the interlobular septa or result in lung fibrosis often result in abnormalities of the subpleural interstitium.
Abnormalities of the subpleural interstitium can be recognized over the costal surfaces of the lung, but are more easily seen in relation to the major fissures, at which two layers of the visceral pleura and subpleural interstitium come in contact. In contrast to conventional CT, in which the obliquely oriented major fissures are usually seen as broad bands of increased or decreased opacity, these fissures are consistently visualized on HRCT as continuous, smooth, and very thin linear opacities. Normal fissures are

less than 1 mm thick, smooth in contour, uniform in thickness, and sharply defined (Figs. 2-2A, 2-10A, and 2-13). The visceral pleura and subpleural interstitium along the costal surfaces of lung are not visible on HRCT in normal subjects.
FIG. 2-16. Anatomy of the pleural surfaces and chest wall.
Parietal Pleura
The parietal pleura, as with the visceral pleura, consists of a mesothelial cell membrane in association with a thin layer of connective tissue. The parietal pleura is somewhat thinner than the visceral pleura, measuring approximately 0.1 mm [33,34]. External to the parietal pleura is a thin layer of loose areolar connective tissue or extrapleural fat, which separates the pleura from the fibroelastic endothoracic fascia and lines the thoracic cavity (Fig. 2-16); the endothoracic fascia is approximately 0.25 mm thick [34,35]. External to the endothoracic fascia are the innermost intercostal muscles and ribs. The innermost intercostal muscles pass between adjacent ribs but do not extend into the paravertebral regions.
As stated in Chapter 1, window level/width settings of 50/350 Hounsfield units (HU) are best for evaluating the parietal pleura and adjacent chest wall. Images at a level of -600 HU with an extended window width of 2,000 HU are also useful in evaluating the relationship of peripheral parenchymal abnormalities to the pleural surfaces [3,36].
On HRCT in normal patients, the innermost intercostal muscles are often visible as 1- to 2-mm-thick stripes (the intercostal stripes) of soft-tissue opacity at the lung-chest wall interface, passing between adjacent rib segments in the anterolateral, lateral, and posterolateral thorax (Fig. 2-17). The parietal pleura is too thin to see on HRCT along the costal pleural surfaces, even in combination with the visceral pleura and endothoracic fascia [37]. However, in the paravertebral regions, the innermost intercostal muscle is anatomically absent, and a very thin line (the

paravertebral line) is sometimes visible at the interface between lung and paravertebral fat or rib (Fig. 2-18) [37]. This line probably represents the combined thickness (0.2 to 0.4 mm) of the normal pleural layers and endothoracic fascia.
FIG. 2-17. Normal intercostal stripe. On high-resolution CT in a normal subject, the intercostal stripe is visible as a thin white line (large arrows). Although it represents the combined thickness of visceral and parietal pleurae, the fluid-filled pleural space, endothoracic fascia, and innermost intercostal muscle, it primarily represents the innermost intercostal muscle. The intercostal stripe is seen as separate from the more external layers of the intercostal muscles because of a layer of intercostal fat. Posteriorly, the intercostal stripe (small arrows) is visible anterior to the lower edge of a rib.
FIG. 2-18. The paravertebral line. In the paravertebral regions (arrows), the innermost intercostal muscle is absent, and, at most, a very thin line (the paravertebral line) is present at the lung-chest wall interface. As in this case, a distinct line may not be seen.
High-Resolution Computed Tomography Measurement of Lung Attenuation
Generally speaking, lung attenuation appears relatively homogeneous on HRCT scans obtained at full inspiration. Measurements of lung attenuation in normal subjects usually range from -700 to -900 HU, corresponding to lung densities of approximately 0.300 to 0.100 g per mL, respectively [38,39]. In a study by Lamers et al. [40], with HRCT obtained using spirometric control of lung volume, the mean lung attenuation measured in 20 healthy subjects at 90% of vital capacity was -859 HU [standard deviation (SD), 39] in the upper lung zones and -847 (SD, 34) in the lower lung zones. A mean lung density of -866 ± 16 HU (range -983 to -824 HU) was found by Gevenois et al. [41] in a study of 42 healthy subjects (21 men, 21 women) from 23 to 71 years of age. In this study, no significant correlation between mean lung density and age was found, but a significant correlation between the total lung capacity, expressed as absolute values and mean lung density was found. A study by Chen et al. [42] of 13 patients with normal pulmonary function tests showed an average lung attenuation of -814 ± 24 HU on HRCT when the entire cross section of lung was used for measurement and an attenuation of -829 ± 21 HU (range, -858 to -770 HU) using three small regions of interest placed in anterior, middle, and posterior lung regions.
An attenuation gradient is normally present, with the most dependent lung regions being the densest, and the least dependent lung regions being the least dense. This gradient is largely caused by regional differences in blood and gas volume that, in turn, are determined by gravity, mechanical stresses on the lung, and intrapleural pressures [36,38]. Differences in attenuation between anterior and posterior lung have been measured in supine patients, and values generally range from 50 to 100 HU [38,43,44], although gradients of more than 200 HU have been reported [43]. The anteroposterior attenuation gradient was found to be nearly linear and was present regardless of whether the subject was supine or prone [43].
Genereux measured anteroposterior attenuation gradients at three levels (aortic arch, carina, and above the right hemidiaphragm) in normal subjects [44]. An anteroposterior attenuation gradient was found at all levels, although the gradient was larger at the lung bases than in the upper lung; the anteroposterior gradient averaged 36 HU at the aortic arch, 65 HU at the carina, and 88 HU at the lung bases. The attenuation gradient was even larger if only cortical lung was considered. Within cortical lung, the attenuation differences at the three levels studied were 45, 81, and 113 HU, respectively.
Vock et al. [38] analyzed CT-measured pulmonary attenuation in children. In general, lung attenuation in children is greater than in adults [38,43], but anteroposterior attenuation gradients were similar to those found in adults, averaging 56 HU at the subcarinal level.
Although most authors have reported that normal anteroposterior lung attenuation gradients are linear, with attenuation increasing gradually from anterior to posterior lung, the lingula and superior segments of the lower lobes can appear relatively lucent in many normal subjects [45]; focal lucency in these segments should be considered a normal finding. Although the reason is unclear, these slender segments may be less well ventilated than adjacent lung and therefore less well perfused, or some air-trapping may be present.
Normal Expiratory High-Resolution Computed Tomography
Expiratory HRCT is generally performed to detect air-trapping in patients with a small airway obstruction or emphysema. On expiratory HRCT, changes in the lung attenuation, cross-sectional area [46], and appearance of airways are typical [47]. Air-trapping of limited extent may also be seen in normals.
Lung Attenuation Changes
Lung parenchyma normally increases in CT attenuation as lung volume is reduced during expiration. This change can generally be recognized on HRCT as an increase in lung opacity (Figs. 2-19, 2-20, and 2-21; see Figs. 1-28, 1-29 1-30) [8,38,43,48,49,50]. Robinson and Kreel [49] found significant inverse correlations between lung volumes determined spirometrically and CT-measured lung attenuation, for the whole

lung (r = -0.680, p >.0005) and for anterior, middle, and posterior lung zones considered individually.
FIG. 2-19. Normal dynamic expiratory HRCT. Inspiratory (A) and expiratory (B) images from a sequence of ten scans obtained during forced expiration in a normal subject. Lung attenuation increases and cross-sectional lung area decreases on the expiratory scan. C: A region of interest has been positioned in the posterior lung, and a time-attenuation curve calculated for this region of interest shows an increase in attenuation from -850 HU to -625 HU from maximal inspiration (I) to maximal expiration (E). Each point on the time density curve represents one image from the dynamic sequence.
The mean attenuation change between full inspiration and expiration ranges from 80 to 300 HU regardless of the expiratory technique used [8,38,40,45,50]. In a study of young, normal volunteers, an increase in lung attenuation averaging 200 HU was consistently seen during forced expiration, but the increase was variable and ranged from 84 to 372 HU [45]. In a study by Chen et al. [42] of patients with normal pulmonary function tests, the average lung attenuation increase on postexpiratory HRCT was 144 ± 47 HU (range, 85 to 235 HU) when three small regions of interest placed in different lung regions were used for measurement and 149 ± 54 HU when the entire cross section of lung was used for measurement. Average lung attenuation on postexpiratory HRCT was -685 HU ± 51 (range, -763 to -580 HU) using three regions of interest and -665 ± 80 HU for the entire cross section of lung [42]. According to Kalender et al., using spirometrically triggered CT [51], a 10% change in vital capacity resulted, on average, in a change of approximately 16 HU, and estimates of lung attenuation at 0% and 100% of vital capacity were -730 HU and -895 HU, respectively. In a study by Lamers et al. [40], with HRCT obtained using spirometric control of lung volume, the mean lung attenuation in 20 healthy subjects measured in the upper lung zones at 90% of vital capacity was -859 HU (SD, 39), whereas at 10% of vital capacity, it was -786 HU (SD, 39). In the lower lung zones, lung attenuation increased from -847 HU (SD, 34) at 90% of vital capacity to -767 HU (SD, 56) at 10% of vital capacity. In a study of spirometrically gated HRCT [52] at 20%, 50%, and 80% of vital capacity, mean lung attenuation measured -747, -816, and -855 HU, respectively. Millar et al. [48] calculated the physical density of lung at full inspiration and expiration, based on the assumption that physical density had

linear relation to radiographic density (physical density = 1 - CT attenuation in HU/1,000) [53]. Using this method, peripheral lung tissue density was measured as 0.0715 g per cm3 (SD, 0.017) at full inspiration and 0.272 g per cm3 (SD, 0.067) at end expiration. Using dynamic expiratory HRCT, a greater increase in lung attenuation may be seen than with static imaging.
FIG. 2-20. Dynamic inspiratory (A) and expiratory (B-C) HRCT in a normal subject, obtained with low (40) mA. On the inspiratory scan (A), lungs appear homogeneous in attenuation. Lung attenuation measured -875 HU in the posterior right lung. During rapid expiration (B), image quality is degraded by respiratory motion. On a scan at maximum expiration (C), lung decreases in volume and increases in attenuation. Posterior dependent lung increases in attenuation to a greater degree than anterior nondependent lung, now measuring -750 HU. Note some anterior bowing of the posterior tracheal membrane, typical of expiratory images.
In children, the CT attenuation of lung parenchyma is higher than in adults and decreases with age [38,43]. Attenuation increases seen with expiration are similar to those found

in adults. Ringertz et al. [54], using ultrafast CT, measured the CT attenuation of children younger than 2.5 years during quiet respiration; the average CT lung attenuation was -551 (SD, 106) on inspiration and -435 HU (SD, 103) on expiration. Vock et al. [38] measured the lung attenuation changes in children ranging in age from 9 to 18 years. Mean lung attenuation at full inspiration and full expiration measured -804 HU and -646 HU, respectively. The anteroposterior attenuation differences were similar to those seen in adults, averaging 56 HU at the subcarinal level, and increased with maximal expiration and increased during expiration [38].
FIG. 2-21. Inspiratory (A) and postexpiratory (B) HRCT in a normal subject. On the expiratory scan, lung increases in attenuation. Posterior dependent lung increases in attenuation to a greater degree than anterior nondependent lung.
Usually, dependent lung regions show a greater increase in lung attenuation during expiration than do nondependent lung regions irrespective of the patient’s position [8,43,45,49,50,55]. As a result, the anteroposterior attenuation gradients normally seen on inspiration are significantly greater on expiratory scans (Fig. 2-21) [38,49,50]; the increase in the anterior-to-posterior attenuation gradient after expiration has been reported to range from 47 to 130 HU in different studies [8,38,45,50]. Furthermore, the expiratory lung attenuation increase in dependent lung regions is greater in the lower lung zones than in the middle and upper zones, probably due to greater diaphragmatic movement or greater basal blood volume [45]. The sum of these changes may be recognizable as increased attenuation or dependent density on supine scans at low lung volume. Although using measurements of attenuation gradients on inspiration and expiration has been investigated as a method of diagnosing lung disease [8,48,56], this technique has not assumed a clinical role.
Normal Air-Trapping
In many normal subjects, areas of air-trapping are visible on expiratory scans (Figs. 2-22 and 2-23); in these regions, lung does not increase normally in attenuation and appears relatively lucent. This appearance is most typically seen in the superior segments of the lower lobes or in the anterior middle lobe or lingula, or it involves individual pulmonary lobules, particularly in the lower lobes [45,57]; it is limited to a small proportion of lung volume. In a study by Chen et al. [42], focal areas of air-trapping, including the superior segments of the lower lobes, were visible in 61% of patients having normal pulmonary function tests. In a study by Lee et al. [57], air-trapping was seen in 52% of 82 asymptomatic subjects with normal pulmonary function tests. The frequency of air-trapping increased with age (p <.05), being seen in 23% of patients aged 21 to 30 years, 41% of those aged 31 to 40 years, 50% aged 41 to 50 years, 65% aged 51 to 60 years, and 76% of those older than 61 years. In another study, discounting the superior segments and air-trapping involving less than two contiguous or five noncontiguous pulmonary lobules, air-trapping was not seen on expiratory

scans in ten healthy nonsmokers, although it was visible in 40% of patients with suspected chronic airways disease who had normal pulmonary function tests [58]. Normal air-trapping is discussed in greater detail in Chapter 3.
FIG. 2-22. Inspiratory (A) and postexpiratory (B) HRCT in a normal subject. On the expiratory scan, there is relative lucency in the superior segments of the lower lobes, posterior to the major fissures. This appearance is normal. Also, focal air-trapping is present in a single lobule (arrow) in the posterior right lung. Note slight anterior bowing of the posterior right bronchus intermedius. This may be seen in some patients on expiration.
Changes in Cross-Sectional Lung Area
The reduction in cross-sectional lung area occurring with expiration has been assessed in several studies and usually ranges from 40% to 50%. In a study of dynamic expiratory HRCT, Webb et al. [45] determined the percent decrease in lung cross-sectional area from full inspiration to full expiration in ten normal volunteers. The area change ranged from 14.8% to 61.3% for all subjects, subject positions, and lung regions. The greatest percentage decrease in cross-sectional area during exhalation occurred in the upper lung zones. This value averaged 51.3% (SD, 6.7) in the supine position and 43.1% (SD, 10.2) in the prone position. The percentage decrease in lung cross-sectional area was least at the lung bases, averaging 30.9% (SD, 7.5) in the supine position and 25.2% (SD, 5) in the prone position. The average area changes for the midlung regions were intermediate between those of upper and lower lung zones, measuring 38.9% (SD, 7.4) in the supine position and 36.7% (SD, 5.3) in the prone position. Similarly, in a study by Lucidarme et al. [58], cross-sectional lung area decreased by an average of 43% (range, 34% to 57%) in a group of ten normal volunteers. Mitchell et al. [46] measured lung area on inspiratory and end expiratory scans at the level of the carina in 78 normal subjects. The percentage change in area from inspiration to expiration averaged 55% (SD, 8.7%).
Changes in cross-sectional lung area during expiration can be related to changes in lung attenuation as shown on HRCT. Simply stated, attenuation increases at the same time that cross-sectional lung area decreases during expiration (Fig. 2-19). For example, Robinson and Kreel [49] found a significant inverse correlation between the expiratory change in cross-sectional lung area measured on CT and changes in CT-measured lung attenuation (r = -0.793, p >.0005). In a study using dynamic expiratory HRCT [45], a correlation between cross-sectional lung area and lung attenuation was found for each of three lung regions evaluated (upper lung, r = 0.51, p = .03; midlung, r = 0.58, p = .01; lower lung, r = 0.51, p = .05). The lower lung zone showed a greater attenuation increase for a given area change; this phenomenon likely reflects the much-greater effect of diaphragmatic elevation on basal lung attenuation than occurs in the upper lungs.
FIG. 2-23. Dynamic expiratory HRCT in a normal subject showing air-trapping in the anterior lingula (arrows) and relative lucency posterior to the left major fissure. Pulmonary lobules in the lung medulla are smaller and less well defined than in the periphery. However, vessels and bronchi in the lung medulla are large and easily seen on HRCT. Note anterior bowing of the posterior wall of the right bronchus.
FIG. 2-24. Normal HRCT appearances of the trachea on inspiratory (A) and expiratory (B) scans. A: On an inspiratory scan shown at a tissue window setting, the trachea appears elliptic. B: After forced expiration, there is marked anterior bowing of the posterior tracheal membrane (arrow) resulting in a decreased anteroposterior diameter. There is little side-to-side narrowing of the tracheal lumen.

Changes in Airway Morphology
The intrathoracic trachea shows significant changes in cross-sectional area, anteroposterior diameter, and transverse diameter from full inspiration to full expiration (Figs. 2-20 and 2-24). In a study using ultrafast dynamic CT in ten healthy men [56], the mean cross-sectional area of the trachea decreased 35% during forced vital capacity maneuver (range, 11% to 61%; SD, 18). The anteroposterior diameter decreased from a mean of 19.6 mm (range, 16.1 to 23.2 mm; SD, 2.3) to 13.3 mm (range, 8.3 to 18.0 mm; SD, 3.5), for a mean decrease of 32%. This change is largely due to an invagination of the posterior tracheal membrane, a finding that is useful in confirming that an adequate expiration has occurred on expiratory CT (Fig. 2-24). The transverse diameter shows less change with expiration; in this study, it decreased from a mean of 19.4 mm (range, 15.2 to 25.3 mm; SD, 2.7) to a mean of 16.9 mm (range, 12.3 to 20.5 mm; SD, 2.6), for a mean decrease of 13%. The change of cross-sectional area correlated strongly with the changes in the anteroposterior and transverse diameters of the trachea (r = 0.88, 0.92; p = .0018, .0002, respectively). The shape of the normal trachea is round or elliptic on inspiration and horseshoe-shaped during and at the end of a full expiration, as the posterior tracheal membrane bows anteriorly.
Morphologic changes in the appearances of bronchi during respiration have not been studied systematically. In our experience, the cross-sectional area of main and lobular bronchi appears slightly reduced on full expiration; some invagination of the posterior wall of the right main bronchus or bronchus intermedius sometimes occurs during forced expiration (Figs. 2-22 and 2-23). Because slightly different levels are usually imaged on the inspiratory and expiratory scans, comparing individual bronchi or specific bronchial levels is often difficult.
1. Müller NL, Miller RR. Computed tomography of chronic diffuse infiltrative lung disease: part 1. Am Rev Respir Dis 1990;142:1206-1215.
2. Müller NL, Miller RR. Computed tomography of chronic diffuse infiltrative lung disease: part 2. Am Rev Respir Dis 1990;142:1440-1448.
3. Webb WR. High-resolution CT of the lung parenchyma. Radiol Clin North Am 1989;27:1085-1097.
4. Zerhouni E. Computed tomography of the pulmonary parenchyma: an overview. Chest 1989;95:901-907.
5. Weibel ER. Looking into the lung: What can it tell us? AJR Am J Roentgenol 1979;133:1021-1031.
6. Murata K, Takahashi M, Mori M, et al. Peribronchovascular interstitium of the pulmonary hilum: normal and abnormal findings on thin-section electron-beam CT. AJR Am J Roentgenol 1996;166:309-312.
7. Lynch DA, Newell JD, Tschomper BA, et al. Uncomplicated asthma in adults: comparison of CT appearance of the lungs in asthmatic and healthy subjects. Radiology 1993;188:829-833.
8. Zerhouni EA, Naidich DP, Stitik FP, et al. Computed tomography of the pulmonary parenchyma: part 2. Interstitial disease. J Thorac Imaging 1985;1:54-64.
9. Weibel ER, Taylor CR. Design and structure of the human lung. In: Fishman AP, ed. Pulmonary diseases and disorders. New York: McGraw-Hill, 1988:11-60.
10. Webb WR, Stein MG, Finkbeiner WE, et al. Normal and diseased isolated lungs: high-resolution CT. Radiology 1988;166:81-87.
11. Murata K, Itoh H, Todo G, et al. Centrilobular lesions of the lung: demonstration by high-resolution CT and pathologic correlation. Radiology 1986;161:641-645.
12. Kim JS, Müller NL, Park CS, et al. Cylindrical bronchiectasis: diagnostic findings on thin-section CT. AJR Am J Roentgenol 1997;168:751-754.

13. Kang EY, Miller RR, Müller NL. Bronchiectasis: comparison of preoperative thin-section CT and pathologic findings in resected specimens. Radiology 1995;195:649-654.
14. Miller WS. The lung. Springfield, IL: Charles C Thomas Publisher, 1947:39-42.
15. Heitzman ER, Markarian B, Berger I, et al. The secondary pulmonary lobule: a practical concept for interpretation of radiographs: II. Application of the anatomic concept to an understanding of roentgen pattern of in disease states. Radiology 1969;93:514-520.
16. Heitzman ER, Markarian B, Berger I, et al. The secondary pulmonary lobule: a practical concept for interpretation of radiographs: I. Roentgen anatomy of the normal secondary pulmonary lobule. Radiology 1969;93:508-513.
17. Miller WS. The lung. Springfield, IL: Charles C Thomas Publisher, 1947:203.
18. Raskin SP. The pulmonary acinus: historical notes. Radiology 1982;144:31-34.
19. Osborne DR, Effmann EL, Hedlund LW. Postnatal growth and size of the pulmonary acinus and secondary lobule in man. AJR Am J Roentgenol 1983;140:449-454.
20. Weibel ER. High resolution computed tomography of the pulmonary parenchyma: anatomical background. Presented at: Fleischner Society Symposium on Chest Disease; 1990. Scottsdale, AZ.
21. Reid L. The secondary pulmonary lobule in the adult human lung, with special reference to its appearance in bronchograms. Thorax 1958;13:110-115.
22. Itoh H, Murata K, Konishi J, et al. Diffuse lung disease: pathologic basis for the high-resolution computed tomography findings. J Thorac Imaging 1993;8:176-188.
23. Reid L, Simon G. The peripheral pattern in the normal bronchogram and its relation to peripheral pulmonary anatomy. Thorax 1958;13:103-109.
24. Gamsu G, Thurlbeck WM, Fraser RG, et al. Peripheral bronchographic morphology in the normal human lung. Invest Radiol 1971;6:161-170.
25. Bergin C, Roggli V, Coblentz C, et al. The secondary pulmonary lobule: normal and abnormal CT appearances. AJR Am J Roentgenol 1988;151:21-25.
26. Hruban RH, Meziane MA, Zerhouni EA, et al. High resolution computed tomography of inflation fixed lungs: pathologic-radiologic correlation of centrilobular emphysema. Am Rev Respir Dis 1987;136:935-940.
27. Heitzman ER. Subsegmental anatomy of the lung. In: The lung: radiologic-pathologic correlations, 2nd ed. St. Louis: Mosby, 1984:42-49.
28. Reid L, Rubino M. The connective tissue septa in the foetal human lung. Thorax 1959;14:3-13.
29. Aberle DR, Gamsu G, Ray CS, et al. Asbestos-related pleural and parenchymal fibrosis: detection with high-resolution CT. Radiology 1988;166:729-734.
30. Fleischner FG. The butterfly pattern of pulmonary edema. In: Frontiers of pulmonary radiology. New York: Grune & Stratton, 1969:360-379.
31. Genereux GP. The Fleischner lecture: computed tomography of diffuse pulmonary disease. J Thorac Imaging 1989;4:50-87.
32. Gurney JW. Cross-sectional physiology of the lung. Radiology 1991;178:1-10.
33. Agostoni E, Miserocchi G, Bonanni MV. Thickness and pressure of the pleural liquid in some mammals. Respir Phys 1969;6:245-256.
34. Bernaudin J-F, Fleury J. Anatomy of the blood and lymphatic circulation of the pleural serosa. In: The pleura in health and disease. New York: Marcel Dekker, 1985:101-124.
35. Policard A, Galy P. La Plevre. Paris: Masson, 1942:23-33.
36. Murata K, Khan A, Herman PG. Pulmonary parenchymal disease: evaluation with high-resolution CT. Radiology 1989;170:629-635.
37. Im JG, Webb WR, Rosen A. Costal pleura: appearances at high-resolution CT. Radiology 1989;171:125-131.
38. Vock P, Malanowski D, Tschaeppeler H, et al. Computed tomographic lung density in children. Invest Radiol 1987;22:627-631.
39. Millar AB, Denison DM. Vertical gradients of lung density in supine subjects with fibrosing alveolitis or pulmonary emphysema. Thorax 1990;45:602-605.
40. Lamers RJ, Thelissen GR, Kessels AG, et al. Chronic obstructive pulmonary diseases. evaluation with spirometrically controlled CT lung densitometry. Radiology 1994;193:109-113.
41. Gevenois PA, Scillia P, de Maertelaer V, et al. The effects of age, sex, lung size, and hyperinflation on CT lung densitometry. AJR Am J Roentgenol 1996;167:1169-1173.
42. Chen D, Webb WR, Storto ML, et al. Assessment of air trapping using postexpiratory high-resolution computed tomography. J Thorac Imaging 1998;13:135-143.
43. Rosenblum LJ, Mauceri RA, Wellenstein DE, et al. Density patterns in the normal lung as determined by computed tomography. Radiology 1980;137:409-416.
44. Genereux GP. Computed tomography and the lung: review of anatomic and densitometric features with their clinical application. J Can Assoc Radiol 1985;36:88-102.
45. Webb WR, Stern EJ, Kanth N, et al. Dynamic pulmonary CT: findings in normal adult men. Radiology 1993;186:117-124.
46. Mitchell AW, Wells AU, Hansell DM. Changes in cross-sectional area of the lungs on end expiratory computed tomography in normal individuals. Clin Radiol 1996;51:804-806.
47. Arakawa H, Webb WR. Expiratory high-resolution CT scan. Radiol Clin North Am 1998;36:189-209.
48. Millar AB, Denison DM. Vertical gradients of lung density in healthy supine men. Thorax 1989;44:485-490.
49. Robinson PJ, Kreel L. Pulmonary tissue attenuation with computed tomography: comparison of inspiration and expiration scans. J Comput Assist Tomogr 1979;3:740-748.
50. Verschakelen JA, Van Fraeyenhoven L, Laureys G, et al. Differences in CT density between dependent and nondependent portions of the lung: influence of lung volume. AJR Am J Roentgenol 1993; 161:713-717.
51. Kalender WA, Rienmuller R, Seissler W, et al. Measurement of pulmonary parenchymal attenuation: use of spirometric gating with quantitative CT. Radiology 1990;175:265-268.
52. Beinert T, Behr J, Mehnert F, et al. Spirometrically controlled quantitative CT for assessing diffuse parenchymal lung disease. J Comput Assist Tomogr 1995;19:924-931.
53. Denison DM, Morgan MDL, Millar AB. Estimation of regional gas and tissue volumes of the lung in supine man using computed tomography. Thorax 1986;41:620-628.
54. Ringertz HG, Brasch RC, Gooding CA, et al. Quantitative density-time measurements in the lungs of children with suspected airway obstruction using ultrafast CT. Pediatr Radiol 1989; 19:366-370.
55. Stern EJ, Webb WR. Dynamic imaging of lung morphology with ultrafast high-resolution computed tomography. J Thorac Imaging 1993;8:273-282.
56. Stern EJ, Graham CM, Webb WR, et al. Normal trachea during forced expiration: dynamic CT measurements. Radiology 1993;187:27-31.
57. Lee KW, Chung SY, Yang I, et al. Correlation of aging and smoking with air trapping at thin-section CT of the lung in asymptomatic subjects. Radiology 2000;214:831-836.
58. Lucidarme O, Coche E, Cluzel P, et al. Expiratory CT scans for chronic airway disease: correlation with pulmonary function test results. AJR Am J Roentgenol 1998;170:301-307.