Lung parenchyma

Mean airstream velocity diminishes as inspiratory flow moves toward the lung parenchyma because of the rapid increase in total cross-sectional area. The largest increases in area occur in the distal bronchioles and pulmonary airways, causing u to approach zero because... 

Mean airflow velocities approach zero as the inspired airstream enters the lung parenchyma, so particle momentum also approaches zero. Most of the particles reaching the parenchyma, however, are extremely fine (< 0.5 pm MMAD), and particle buoyancy counteracts gravitational forces. Temperature gradients do not exist between the airstream and airway wall because the inspired airstream has been warmed to body temperature and fully saturated before reaching the parenchyma. Consequently, diffusion driven by Brownian motion is the only deposition mechanism remaining for airborne particles. Diffusivity, can be described under these conditions by... 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

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. 

C. neoformans is strongly neurotropic and readily disseminates from the lung to the CNS, specifically the lep-tomeninges, and occasionally the parenchyma of the brain. The clinical characteristics of cryptococcal meningitis differ somewhat, however, between patients with and without underlying AIDS. In patients without AIDS, disease presentation is more insidious and symptoms such as dizziness,... 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... 

The most common etiology is exposure to environmental tobacco smoke, but other chronic inhalational exposures can also lead to COPD. Inhalation of noxious particles and gases stimulates the activation of neutrophils, macrophages, and CD8+ lymphocytes, which release a variety of chemical mediators, including tumor necrosis factor-a, interleukin-8, and leukotriene B4. These inflammatory cells and mediators lead to widespread destructive changes in the airways, pulmonary vasculature, and lung parenchyma. 

Huh JC, Strickland DH, Jahnsen FL, Turner DJ, Thomas JA, Napoli S, Tobagus I, Stumbles PA, Sly PD, Holt PG Bidirectional interactions between antigen-bearing respiratory tract dendritic cells (DCs) and T cells precede the late phase reaction in experimental asthma DC activation occurs in the airway mucosa but not in the lung parenchyma. J Exp Med 2003 198 19-30. 

Casolaro V, Gale D Functional comparisons of cells obtained from peripheral blood, lung parenchyma, bronchoalve-olar lavage in asthmatics. Am Rev Respir Dis 1989 139 1375-1382. 

Aizawa, H., Inoue, H., Matsumoto, K., Koto, H., Nakano, H., and Kara, N. (1996) Thromboxane A antagonist inhibits leukotriene D -induced smooth muscle contraction in guinea-pig lung parenchyma, but not in trachea. Prostaglandins Leukot. Essent. Fatty Acids. 55,437-440. 

An appreciable body of evidence has accumulated to indicate that ozone has extrapulmonary effects. Although some of the reported effects may be secondary to the reaction of ozone with intrapulmonary neural receptors or to release of humoral substances from the lung, other finding appear to be mote directly related to an oxidizing effect of ozone. The biochemical basis for the latter is unclear, particularly because the reactivity of ozone and its short-lived intermediates would make it unlikely for them to penetrate the pulmonary parenchyma. Earlier studies on the subject of extrapulmonary effects have been reviewed by Stokinger. ... 

Designation of intrathoracic or abdominal tumors as mesotheliomas is not straightforward. A mesothelial mesothelioma may be difficult to distinguish from a peripheral bronchogenic carcinoma partly because of the nature of the clinical course of the diseases as well as their similar location. Mesothelioma spreads extensively on the pleura, is usually unresectable, and responds poorly to chemotherapy or radiation. In all of these respects it is identical to peripheral carcinoma of the lung parenchyma, which may spread to the pleura. The diagnostic distinction, perhaps somewhat academic (Gaenslcr et ah, 1985), must go beyond clinical evaluation to tissue examination. 

Pneumoconioses Lung disease caused by the permanent deposition of particulates within the lung parenchyma. 

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... 

No degenerative changes in the pulmonary parenchyma were found, but 7/20 mice that died 15 months after intravenous injection of Thorotrast (Guimaraes et al. 1955) and 8/20 mice that were sacrificed 5-12 months after injection of Thorotrast (Guimaraes and Lamerton 1956) had lung adenomas. There was no significant difference in survival between the treated and control animals in either study. In a few cases, an association between the presence of Thorotrast deposits in the lungs and the proliferation of bronchioles and alveoli was found. 

The benefits of the use of (3-blockade appear to exceed by far the risks of bronchospasm in patients diagnosed with chronic obstructive pulmonary disease (COED) and/or suppression of hypoglycemic responses in diabetics. COPD is very different from bronchospas-tic asthma. Young people with asthma have highly reactive airways and can die within hours of a bronchospasm in response to an exposure to an external agent. This highly reversible dynamic condition contrasts sharply with the destruction of connective tissue in lung parenchyma and dead airway sacs that are not very reactive. This is a very different phenomenon. 

L C. Inflammation of the airway is a hallmark of asthma. The use of antiinflammatory drugs, such as inhaled corticosteroids, is critical to the long-term control of asthma. No credible data indicate either that asthma is psychosomatic or that it develops in response to vaccinations against childhood diseases. Asthma is a disease limited to the airways. It does not involve the lung parenchyma. Although upper respiratory tract infections can exacerbate asthma symptoms, asthma is not caused by infection, nor is it communicable. 

Male Wistar rats exposed to 243 ppm [437 mg/m ] acetaldehyde atmospheres for 8 h per day on five days per week for five weeks showed increases in functional residual capacity, residual volume, total lung capacity and respiratoiy frequency. These changes were interpreted as being caused by damage to the peripheral regions of the lung parenchyma (Saldiva et al., 1985). 

De Flora, S., Bennicelli, C., Zanacchi, P., Camoirano, A., Petruzzelli, S. Giuntini, C. (1984) Metabolic activation and deactivation of mutagens by preparations of human lung parenchyma and bronchial tree. Mutat. Res., 139, 9-14... 

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