肺生长和肺泡增生。

Pathobiology annual Pub Date : 1975-01-01
W M Thurlbeck
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引用次数: 0

摘要

随着肺从婴儿期到成年期的体积增长,大量的组织被添加到肺中,这主要是肺泡增殖的结果。物种差异可能存在:小鼠和大鼠出生时没有肺泡,但通常认为人类出生时存在肺泡。肺泡增殖是由原始末端单位的细分、原发性肺囊、继发性肺泡嵴以及非肺泡和部分肺泡气道的肺泡化引起的。肺泡发育的确切方法和上述肺泡生长模式的相对重要性尚不清楚。在大鼠和小鼠出生的最初几天,有一个肺扩张的阶段,随后是细胞和组织快速增殖的阶段。随后肺发生重塑,此时肺组织增加较少,扩张更为突出;这导致肺泡壁的拉伸。在大鼠的一生中,肺泡增殖可能发生。在人类受试者中,肺泡增殖在生命的最初几年是最快的。在此之后,它似乎变慢,并可能在8岁时停止,尽管有一些迹象表明,肺泡增殖可能会持续到体细胞生长停止。由于细胞增生,全肺切除术使对侧肺组织增大和增加。肺泡增生可能不会发生。如果胸壁畸形发生在婴儿期或宫内期,胸内容积的减少会导致肺变小,人的肺泡也可能过少。在高海拔地区,人的肺大而重,可能比正常人有更多的肺泡。
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Lung growth and alveolar multiplication.

As the lung grows in volume from infancy to adult life, considerable amounts of tissue are added to the lung, mostly as a result of alveolar multiplication. Species differences may exist: at birth alveoli are absent in mice and rats but alveoli are generally thought to be present in humans at birth. Alveolar multiplication is brought about by the subdivision of the primitive terminal units, primary pulmonary saccules, by secondary alveolar crests, and by alveolarization of nonalveolated and partly alveolated airways. The exact method of alveolar development and the relative importance of the above modes of alveolar growth are not known. In the first few days of life in rats and mice, there is a phase of dilatation of the lung, followed by a phase of rapid cellular and tissue proliferation. Subsequently, remodeling of the lung occurs, during which stage lung tissue increases little and dilatation is more prominent; this leads to stretching of the alveolar walls. Alveolar multiplication may occur throughout life in the rat. In human subjects, alveolar multiplication is most rapid in the first few years of life. After this, it appears to slow and perhaps stop by age 8 years, although there is some suggestion that alveolar multiplication may continue until somatic growth stops. Pneumonectomy produces enlargement and increase in tissue of the contralateral lung by virtue of cellular hyperplasia. Alveolar multiplication likely does not occur. Diminution of intrathoracic volumes produces small lungs which, in the human, may also have too few alveoli if the chest wall deformity has its onset in infancy or in intrauterine life. High altitude produces large, heavy lungs which may have more alveoli than normal.

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