Quantitative characteristics of the Feyrter (APUD) cells of the neonatal rabbit lung in normoxia and chronic hypoxia.

Hernández-Vásquez, Aureliano; Will, James A.; Quay, W. B.

doi:10.1136/thx.32.4.449

Cited by 49 publications

(4 citation statements)

References 31 publications

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“…We, therefore, chose to express simply numbers of endocrine cells per square cm of tissue section. This method is generally less accurate than those discussed above but has been used frequently in the past (Hernandez-Vasquez. Will & Quay 1977,Taylor 1977.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary endocrine cells in hypertensive pulmonary vascular disease

Heath¹,

Yacoub²,

Gosney³

et al. 1990

Histopathology

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A study was made of the number of pulmonary endocrine cells, immunoreactive for gastrin-releasing peptide (bombesin) or calcitonin, in the terminal bronchioles of 39 cases of pulmonary vascular disease. In 25 of these, the form of vascular disease was plexogenic pulmonary arteriopathy, primary in 12 and secondary in 13, while the remaining 14 subjects had a wide range of other varieties of hypertensive pulmonary vascular disease. We found that pulmonary endocrine cells, especially those containing bombesin, were increased in number in both the primary and secondary forms of plexogenic pulmonary arteriopathy but not in other varieties of pulmonary hypertension. The prominent bombesin-containing cells were found in cases with cellular plexiform lesions but occurred even more prominently at an earlier stage when vascular smooth muscle cells were migrating from the inner media into the intima.

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Section: Discussionmentioning

confidence: 99%

Pulmonary endocrine cells in hypertensive pulmonary vascular disease

Heath¹,

Yacoub²,

Gosney³

et al. 1990

Histopathology

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“…In these species the anterior mucosa of the trachea reveals more NECs than the posterior mucosa, and the greatest concentration of cells can be found in the cranial, extrathoracic segment. In addition to the trachea [165,[167][168][169], NECs are found distributed throughout the bronchi and terminal bronchioles [106,158,[170][171][172][173]. In rats, the cells are most predominant in the trachea and gradually decrease in density toward more distal regions [131,143].…”

Section: Vascular Changes Associated With 'Neurogenic Inflammation' Mmentioning

confidence: 99%

Pathways Underlying Afferent Signaling of Bronchopulmonary Immune Activation to the Central Nervous System

Hale

Rook

Lowry

2012

Chemical Immunology and Allergy

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Bronchopulmonary inflammation, such as that associated with asthma, activates afferent neural pathways. We recently demonstrated that localized inflammation in the lungs, induced by intratracheal administration of ovalbumin in ovalbumin-preimmunized mice (an animal model of asthma) results in activation of the dorsolateral part of the nucleus of the solitary tract, a major target of vagal afferent fibers innervating the lungs and airways. Activation of the nucleus of the solitary tract was evident in the absence of activation of the area postrema, a circumventricular organ, consistent with the hypothesis that localized inflammation in the bronchopulmonary system can signal to the central nervous system via specific neural pathways, in the absence of circulating proinflammatory mediators. The pattern of brain activation in ovalbumin-challenged mice differs from the pattern of activation in mice challenged with heat-killed Mycobacterium vaccae, suggesting that qualitative aspects of bronchopulmonary inflammation determine the overall pattern of brain activation. The mechanisms through which localized bronchopulmonary inflammation signals to the central nervous system is poorly understood, but appears to involve both vagal and spinal afferent pathways. In this chapter, we review our current understanding of the anatomical pathways through which localized inflammation in the bronchopulmonary system influences central nervous system function.

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“…Studies of the effect of hypoxia on endocrine cells have been made using argyrophilia or formalin-induced fluorescence to detect the cells, but the results are conflicting. Some authors found an increase in cell numbers (Taylor, 1977;Pack et al, 1986) and suggested that hyperplasia of endocrine cells may be occurring; others found no change (Moosavi et al, 1973;Hernandez-Vasquez, 1977;.…”

mentioning

confidence: 95%