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Alveolar parenchyma

Hind et al. (2002) described the temporal and spatial expression of the retinoid-synthesizing enzymes Aldh-1 and Raldh-2 in the postnatal mouse lung. Both enzymes are upregulated during the period of maximal alveolar wall cell proliferation. Aldh-1 is located in the bronchial epithehum and alveolar parenchyma, and Raldh-2 is restricted to the bronchial epithelium and pleural mesothelial cells. [Pg.170]

Proteinases and antiproteinases are part of the normal protective and repair mechanisms in the lungs. The imbalance of proteinase-antiproteinase activity in COPD is a result of either increased production or activity of destructive proteinases or inactivation or reduced production of protective antiproteinases. AAT (an antiproteinase) inhibits trypsin, elastase, and several other proteolytic enzymes. Deficiency of AAT results in unopposed proteinase activity, which promotes destruction of alveolar walls and lung parenchyma, leading to emphysema. [Pg.232]

Particles deposited on or in the lung parenchyma are cleared primarily by alveolar macrophages. These phagocytized particles migrate to the ciliated epithelium or to the... [Pg.7]

The transition zone consists of the respiratory bronchioles (generations 17 to 19), which contain alveoli. At the terminal end, the respiratory zone is composed of parenchyma that contains the alveolar ducts and about 300 million alveoli (alveolar sacs) to provide the gas-exchange surface. Since the surface area expands to such a large extent within the very last generations of bifurcations, the inhalation airflow rapidly slows down to zero velocity so that the movement of gas molecules and the exchange occurs entirely by diffusion (Stocks and Hisloop 2002). [Pg.241]

For humans, the overall chromium(VI)-reducing/sequestering capacities were estimated to be 0.7-2.1 mg/day for saliva, 8.3-12.5 mg/day for gastric juice, 11-24 mg for intestinal bacteria eliminated daily with feces, 3,300 mg/hour for liver, 234 mg/hour for males and 187 mg/hour for females for whole blood, 128 mg/hour for males and 93 mg/hour for females for red blood cells, 0.1-1.8 mg/hour for ELF, 136 mg/hour for pulmonary alveolar macrophages, and 260 mg/hour for peripheral lung parenchyma. Although these ex vivo data provide important information in the conversion of chromium(VI) to reduced states, the values may over or under estimate the in vivo reducing capabilities (De Flora et al. 1997). [Pg.173]

Capillary endothelial cells comprise 30-42% of cells in the alveolar region and comprise the walls of the extensive network of blood capillaries in the lung parenchyma. The endothelium forms a continuous, attenuated cell layer that transports respiratory gases, water, and solutes. However, it also forms a barrier to the leakage of excess water and macromolecules into the pulmonary interstitial space. Pulmonary endothelial cells, like type I cells, are vulnerable to injury from inhaled substances and substances in the systemic circulation. Injury to the endothelium results in fluid and protein leakage into the pulmonary interstitium and alveolar spaces, resulting in pulmonary edema. [Pg.647]

A number of factors determine whether tissue in the lung parenchyma is successfully repaired after injury or whether an inflammatory response progresses to a pathologic outcome. As mentioned previously, the alveolar region is especially vulnerable to damage due to the delicate architecture of the type I epithelium and blood capillary endothelial membranes. An appropriate balance of catabolic and... [Pg.650]

An increase in the total numbers of T-Iymphocytes is observed in lung parenchyma as well as in peripheral and central airways of patients with COPD a greater increase is observed in CD8 than CD4+ cells (6, 24). A correlation is observed between the numbers of T-cells and the amount of alveolar destruction and the severity of airflow obstruction. Furthermore, the oifly significant difference in the inflammatory cell infiltrate in asymptomatic smokers and smokers with COPD is an increase in T-cells, maiifly CD8+, in patients with COPD. An increase in the absolute number of CD4+ T-cells, albeit in smaller numbers, is evidenced in the airways of smokers with COPD, and these cells express activated STAT-4, which is a transcription factor that is essential for activation and commitment of the Thl lineage, and IFN-y. [Pg.2307]

Macs are ubiquitous throughout the respiratory tract, and discrete populations can be discerned in the airway mucosa, the lung parenchyma ( interstitial macrophages IMs), the luminal surface of the alveoli (pulmonary alveolar macrophages PAMs) and the conducting airways, and in the vascular bed ( intravascular macrophages IVMs). The latter represent a stable marginated population, intimately associated with the endothelial basement membrane they are most common in ruminants (Winkler, 1989) but also occur in humans. [Pg.2]

The pulmonary region includes the functional gas exchange sites of the lung. The terminal bronchioles of the TB tree branch to form the respiratory bronchioles. The major structural elements of the parenchyma of this region of the lung include the alveolar ducts, alveolar sacs, alveolar capillaries, and pulmonary lymphatics. The walls of the tubular alveolar ducts are covered with alveoli. As these branch, they... [Pg.2261]

Study of tissue samples from lungs of Iranian casualties who died as a result of exposure to mustard gas has revealed a pattern identical with that described above. In all, tissue from four patients was studied. Alveolar capillary congestion, haemorrhage, oedema, the formation of hyaline membranes and fibrosis were seen. The casualties died as a result of multi-system organ failure and the changes in the lung parenchyma were very similar to those seen in cases of Adult Respiratory Distress Syndrome (ARDS) (Maynard, unpublished observations). [Pg.393]

Morphologically, emphysema is associated with a destruction of the alveolar septum, which results in a dilation and consequent enlargement of the alveolar spaces (Fig. 19). This is apparently caused by a breakdown of the interstitial connective tissue proteins (primarily elastin) that provide the major structural framework of the lung parenchyma. Two types of emphysema have been defined on the basis of the types of destruction of the alveolar septa observed and the type of dilation of the terminal respiratory unit (the acini) that is observed. A typical acinus branches from a terminal bronchiole and consists of the respiratory bronchioles that have alveolated walls and lead to the alveolar ducts and ultimately to the alveolar sacs (see Fig. 3). In centrilobular (or centriacinar) emphysema, the sites of degradation and dilation are limited to the region of the terminal and respiratory bronchioles. In panlobular (or panacinar) emphysema, the entire acinus (including the alveolar ducts and sacs) is more uniformly affected. [Pg.338]


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See also in sourсe #XX -- [ Pg.476 ]




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