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Terminal bronchioles

Conducting Bronchiole Terminal Bronchiole Respiratory Bronchiole Alveolar Duct... [Pg.24]

The lung. The middle diagram is a close-up view of the end of a bronchiole. Each bronchiole terminates in many alveolar sacs. The diagram on the right is a close-up view of an alveolus. The cell membrane of each alveolus is very thin and surrounded by many blood capillaries, thereby allowing for rapid exchange of oxygen for carbon dioxide, as well as absorption of other substances. [Pg.295]

Bronchioles, terminal bronchioles 12-16 1.0-0.4 Ciliated cuboidal cell Clara cell Serous cell 10... [Pg.213]

Allergic alveolitis An allergic response to inhalation of organic particles that involves inflammation of the small terminal branches of the bronchioles. Symptoms include coughing, increased production of mucus, fever, fatigue, and muscle aches. [Pg.1413]

Bronchioles The very small airways of the lungs that terminate in the alveoli. [Pg.1418]

A condition of the lung characterized by abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis. [Pg.463]

Other disorders of the lower respiratory tract include emphysema (lung disorder in which the terminal bronchioles or alveoli become enlarged and plugged with mucus) and chronic bronchitis (chronic inflammation and possibly infection of die bronchi). Chronic obstructive pulmonary disease (COPD) is die name given collectively to emphysema and chronic bronchitis because die obstruction to die airflow is present most of the time. Asdima diat is persistent and present for most of die time may also be referred to as COPD. [Pg.333]

COPD includes chronic bronchitis and emphysema. Chronic bronchitis is defined clinically as a chronic productive cough for at least 3 months in each of two consecutive years in a patient in whom other causes have been excluded.1 Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis.1 The major risk factor for both conditions is cigarette smoking, and many patients share characteristics of each condition. Therefore, new consensus guidelines have moved away from using these subsets and instead focus on chronic airflow limitation. [Pg.231]

Branching from the terminal bronchioles are the respiratory bronchioles. This is the first generation of airways to have alveoli in their walls. Finally, there are the alveolar ducts which are completely lined with alveolar sacs. This region, from the respiratory bronchioles through the alveoli, is referred to as the respiratory zone, which comprises most of the lungs and has a volume of about 3000 ml at the end of a normal expiration. [Pg.241]

The volume of the conducting airways that does not contain any respiratory epithelium. This stretches from the nasal cavity to the generation 16 terminal bronchioles (ml). [Pg.128]

In studies on hamsters and guinea pigs exposed to aerosols of crude and refined extracts from cotton mill trash and CMD, Kilburn et al (59) has further demonstrated recruitment of PMN beneath the basement membrane and on luminal surfaces of intrapulmonary airways and tracheas. When administered as aerosols or dust, polyphenolic extracts from cotton trash and pure and oxidization-polymerization products of quercetin also recruit PMN from the trachea to terminal bronchioles in hamsters (60). [Pg.180]

The sites of action and effects of ozone and other photochemical oxidants are described in Chapters 8 and 9. Recent work with primates has suggested that ozone is absorbed along the entire respiratory tract, penetrates more into the peripheral nonciliated airways, and causes more lesions in the respiratory bronchioles and alveolar ducts as the inhaled ozone concentration increases from 0.2 to 0.8 ppm. The most common and most severe tissue damage was observed in the respiratory bronchioles. The ciliated cells in the terminal bronchioles and the Type 1 cells in the epithelial layer of the proximal alveoli of rats were the... [Pg.281]

Continuous for 18 months Thickening of terminal and respiratory bronchioles barely noticeable at 1 ppm at 3 ppm. formation of peribronchiolar collars with resulting narrowing of small airways Dog 73... [Pg.373]

Fig. 3.1 Schematic diagram of the human respiratory system. The gross anatomy of the lung, the covering membranes (pleura), airways and air sacs (alveoli) are shown. The average diameter of portions of the air flow system are indicated trachea, 20 mm bronchus, 8 mm terminal and respiratory bronchioles, 0.5 mnn alveolar duct, 0.2 mm alveolar sacs, 0.3 mm. Fig. 3.1 Schematic diagram of the human respiratory system. The gross anatomy of the lung, the covering membranes (pleura), airways and air sacs (alveoli) are shown. The average diameter of portions of the air flow system are indicated trachea, 20 mm bronchus, 8 mm terminal and respiratory bronchioles, 0.5 mnn alveolar duct, 0.2 mm alveolar sacs, 0.3 mm.
Rats exposed to 42,000 ppm became hyperactive within the first 7 minutes, and at the end of 7 minutes they appeared lethargic and ataxic. After 95 minutes, the animals were completely anesthetized. There was no mortality when the exposure was terminated at the end of 5 hours, and most of the animals recovered completely within 40 minutes. Edema and alveolar hemorrhage were present in animals killed at termination of the single exposure, whereas bronchiolitis and pneumonitis were observed in rats killed 9 days after exposure. [Pg.450]

XB = tracheobronchial (trachea, bronchi, bronchioles to terminal bronchioles) pu = pulmonary (respiratory bronchioles, alveolar region)... [Pg.153]

NT207 Chang, W. C., Y. C. Lee, C. L. Liu, et al. Increased expression of iNOS and c-fos via regulation of protein tyrosine phosphorylation and MEK1/ERK2 proteins in terminal bronchiole lesions in the lungs of rats exposed to cigarette smoke. Arch Toxicol 2001 75(1) 28-35. [Pg.351]


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See also in sourсe #XX -- [ Pg.271 , Pg.272 ]




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