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肺泡上皮转运的超微结构特征。

Ultrastructural features of alveolar epithelial transport.

作者信息

DeFouw D O

出版信息

Am Rev Respir Dis. 1983 May;127(5 Pt 2):S9-13.

PMID:6846951
Abstract

The permeability of the alveolar epithelium is considerably less than the capillary endothelium, although macromolecules can traverse the epithelial lining of alveoli. Knowledge of the contributions of potential surface domains within the epithelial glycocalyx and of the surfactant lining layer to the differences in epithelial and endothelial permeabilities across the air-blood barrier is not secure. Increased numbers of type I vesicles and depletion of type II lamellar bodies characterize the alveolar epithelium after the development of septal edema and alveolar flooding. The thick sides of the alveolar septa are the sites of interstitial fluid accumulation and of increased attentuation along the surface of type I cells in edematous lungs. The development of septal edema and alveolar flooding at 15 degrees C, on the other hand, is not associated with increased vesicles or depletion of lamellar body contents. Thus, these concomitant cellular changes are not primarily associated with formation of alveolar edema but more likely are response to the distension of the septal interstitium and alveoli. The type II cell response could signify an attempt to replenish the surface active phospholipids after alveolar flooding. The vesicular response could represent a cellular defense mechanism against excessive interstitial fluid accumulation by providing a pathway for the return of excess filtrate to the blood (via an expanded endothelial vesicle population) or to the alveolar hypophase layer. The increased vesicle population, on the other hand, could signify an initial cellular pathologic response, with subsequent coalescence of the more closely packed vesicles leading to the formation of cytoplasmic vacuoles and finally to epithelial disruption.

摘要

肺泡上皮的通透性远低于毛细血管内皮,尽管大分子物质能够穿过肺泡的上皮衬里。目前尚不清楚上皮糖萼内潜在表面结构域以及表面活性物质衬里层对气血屏障上皮和内皮通透性差异的作用。在间隔性水肿和肺泡积水形成后,I型囊泡数量增加和II型板层小体减少是肺泡上皮的特征。肺泡间隔的厚侧是水肿肺中间质液积聚的部位,也是I型细胞表面衰减增加的部位。另一方面,15摄氏度时间隔性水肿和肺泡积水的发展与囊泡增加或板层小体内容物减少无关。因此,这些伴随的细胞变化并非主要与肺泡水肿的形成有关,而更可能是对间隔间质和肺泡扩张的反应。II型细胞反应可能意味着肺泡积水后试图补充表面活性磷脂。囊泡反应可能代表一种细胞防御机制,通过为多余滤液返回血液(通过增加的内皮囊泡群体)或肺泡液相层提供途径,来对抗过多的间质液积聚。另一方面,增加的囊泡群体可能意味着最初的细胞病理反应,随后紧密堆积的囊泡融合导致细胞质空泡形成,最终导致上皮破坏。

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