The Cytology of the Lung: Ultrastructure of the Respiratory Epithelium and Extracellular Lining Layers

1982 ◽

Vol 40 ◽

pp. 248-249

Author(s):

M.R. Richter ◽

R.V. Blystone

Keyword(s):

Lung Development ◽

Critical Role ◽

Respiratory Epithelium ◽

Chick Embryos ◽

Embryonic Chick ◽

White Leghorn ◽

Lung Maturation ◽

Synthetic Analogs ◽

Lung Physiology ◽

Avian Lung

Dexamethasone and other synthetic analogs of corticosteroids have been employed clinically as enhancers of lung development. The mechanism(s) by which this steroid induction of later lung maturation operates is not clear. This study reports the effect on lung epithelia of dexamethasone administered at different intervals during development. White Leghorn chick embryos were used so as to remove possible maternal and placental influences on the exogenously applied steroid. Avian lung architecture does vary from mammals; however, respiratory surfactant produced by the lung epithelia serves an equally critical role in avian lung physiology.

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Ultrastructure of pulmonary microvasculature in acute endotoxemia

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100083217 ◽

1978 ◽

Vol 36 (2) ◽

pp. 470-471

Author(s):

R. G. Gerrity ◽

M. Richardson

Keyword(s):

Polymorphonuclear Leukocytes ◽

Alveolar Epithelium ◽

Endothelial Damage ◽

Capillary Endothelium ◽

Type Ii Cells ◽

Type Ii ◽

Interstitial Edema ◽

Pulmonary Capillaries ◽

Lung Ultrastructure ◽

Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

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Bronchial stereocilia in the immotile cilia syndrome: A case report

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100110635 ◽

1984 ◽

Vol 42 ◽

pp. 52-53

Author(s):

George Price ◽

Lizardo Cerezo

Keyword(s):

Surface Modifications ◽

Respiratory Epithelium ◽

Immotile Cilia ◽

Kartagener's Syndrome ◽

Membrane Blebs ◽

Radial Spokes ◽

Males And Females ◽

Dynein Arms ◽

Ultrastructural Finding ◽

Ultrastructural Findings

Ultrastructural defects of ciliary structure have been known to cause recurrent sino-respiratory infection concurrent with Kartagener's syndrome. (1,2,3) These defects are also known to cause infertility in both males and females. (4) Overall, the defects are defined as the Immotile, or Dyskinetic Cilia Syndrome (DCS). Several ultrastructural findings have been described, including decreased number of cilia, multidirection orientation, fused and compound cilia, membrane blebs, excess matrix in the axoneme, missing outer tubular doublets, translocated doublets, defective radial spokes and dynein arms. A rare but noteworthy ultrastructural finding in DCS is the predominance of microvilli-like structures on the luminal surface of the respiratory epithelium. (5,6) These permanent surface modifications of the apical respiratory epithelium no longer resemble cilia but reflect the ultrastructure of stereocilia, similar to that found in the epidydimal epithelium. Like microvilli, stereocilia are devoid of microtubular ultrastructure in comparison with true cilia.

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Eupatoriopicrin may modulate lipopolysaccharide-induced inflammation in human respiratory epithelium

10.1055/s-0039-3400034 ◽

2019 ◽

Author(s):

B Gierlikowska ◽

W Gierlikowski ◽

K Broniarek ◽

AK Kiss

Keyword(s):

Respiratory Epithelium

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THE CYTOLOGIC DISTINCTION BETWEEN BRONCHOALVEOLAR CARCINOMA AND REACTIVE/REPARATIVE RESPIRATORY EPITHELIUM

Southern Medical Journal ◽

10.1097/00007611-199510001-00179 ◽

1995 ◽

Vol 88 ◽

pp. S81

Author(s):

Steven D. Gurley ◽

Russell M. Fiorella

Keyword(s):

Respiratory Epithelium

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Mucosal Changes in the Trachea and Main Bronchi of Newborn Infants after Nasotracheal Intubation

Anaesthesia and Intensive Care ◽

10.1177/0310057x7500300306 ◽

1975 ◽

Vol 3 (3) ◽

pp. 209-217 ◽

Cited By ~ 7

Author(s):

G. C. Fisk ◽

W. de C. Baker

Keyword(s):

Endotracheal Tube ◽

Main Bronchus ◽

Squamous Metaplasia ◽

Nasotracheal Intubation ◽

Newborn Infants ◽

Respiratory Epithelium ◽

Lower Trachea ◽

Nasotracheal Tube ◽

Mucosal Changes ◽

The Right

Permanent sequelae of nasotracheal intubation are uncommon, but acute ulceration and squamous metaplasia occur. Histological sections from the trachea and main bronchi were examined in 12 infants. A nasotracheal tube had been inserted during the first two weeks of life of these infants and had been in place for more than one week. In four cases the patient died some time (7 to 108 days) after extubation. Similar sections from patients who were not intubated, intubated only for attempted resuscitation, or intubated for several hours were studied for comparison. The sections were classified according to the degree of mucosal loss and metaplasia, and the extent of the lesions was estimated. Squamous change was seen in most sections from all 12 patients with the exception of one who died 57 days after extubation. Some respiratory epithelium was seen in all patients. In the eight patients who died while intubated, the changes were more marked in the right main bronchus than the left in seven, and more marked in the lower trachea than the upper in five. In the two patients intubated for several hours, in addition to mucosal loss, early metaplasia was seen. It is suggested that mucosal loss is replaced by the squamous metaplasia, and that trauma caused by suction catheters in the lower trachea and right main bronchus is more extensive than that due to the endotracheal tube itself.

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