scholarly journals Application of Morphometric and Stereological Techniques on Analysis and Modelling of the Avian Lung

2017 ◽  
Author(s):  
John N. Maina
Keyword(s):  
Avian Lung

Dexamethasone Effect on Embryonic Chick Respiratory Epithelium

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.

Branching morphogenesis in the avian lung: electron microscopic studies using cationic dyes

Development ◽  
1986 ◽  
Vol 94 (1) ◽  
pp. 189-205
Author(s):  
Betty C. Gallagher
Keyword(s):  
Tannic Acid ◽  
Basal Lamina ◽  
Branching Morphogenesis ◽  
Ruthenium Red ◽  
Interparticle Spacing ◽  
Blue Staining ◽  
Mouse Lung ◽  
Alcian Blue Staining ◽  
Electron Microscopic ◽  
Avian Lung

The developing chick lung was examined in the electron microscope for intimate cell contacts between epithelium and mesenchyme, discontinuities in the basal lamina and substructure of the basement membrane. Cell filopodia were seen which crossed the basal lamina from both the epithelial and the mesenchymal cells. Ruthenium red and tannic acid staining of the basal lamina of the chick lung showed it to be thin and sometimes discontinuous at the tips compared to the more substantial basal lamina in the interbud areas. The bilaminar distribution of particles seen with ruthenium red is similar to those seen in the cornea and lens. With tannic acid staining, filaments could be seen which crossed the lamina lucida and connected with the lamina densa. Spikes perpendicular to the basal lamina were sometimes seen with a periodicity of approximately 110 nm. Alcian blue staining revealed structure similar to that seen by ruthenium red staining in the salivary and mammary glands, although the interparticle spacing was closer. Collagen was located in areas of morphogenetic stability, as has been seen by other investigators in different tissues. Collagen was coated with granules (probably proteoglycan) at periodic intervals when stained with ruthenium red. The fibrils were oriented circumferentially around the mesobronchus and were assumed to continue into the bud, but the fibres curve laterally at the middle of a bud. This orientation is opposite to that seen by another investigator in the mouse lung. In general, the observations made in the avian lung are similar to those seen in branching mammalian tissue. It is likely, therefore, that the chick lung uses strategies in its morphogenesis that are similar to those that have been elucidated previously in developing mammalian organs.

scholarly journals Development and Remodeling of the Vertebrate Blood-Gas Barrier

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Andrew Makanya ◽  
Aikaterini Anagnostopoulou ◽  
Valentin Djonov
Keyword(s):  
Extracellular Proteins ◽  
Appreciable Amount ◽  
Interstitial Tissue ◽  
Type I ◽  
Blood Gas ◽  
Gas Barrier ◽  
Molecular Control ◽  
Blood Capillaries ◽  
Mammalian Lung ◽  
Avian Lung

During vertebrate development, the lung inaugurates as an endodermal bud from the primitive foregut. Dichotomous subdivision of the bud results in arborizing airways that form the prospective gas exchanging chambers, where a thin blood-gas barrier (BGB) is established. In the mammalian lung, this proceeds through conversion of type II cells to type I cells, thinning, and elongation of the cells as well as extrusion of the lamellar bodies. Subsequent diminution of interstitial tissue and apposition of capillaries to the alveolar epithelium establish a thin BGB. In the noncompliant avian lung, attenuation proceeds through cell-cutting processes that result in remarkable thinning of the epithelial layer. A host of morphoregulatory molecules, including transcription factors such as Nkx2.1, GATA, HNF-3, and WNT5a; signaling molecules including FGF, BMP-4, Shh, and TFG-βand extracellular proteins and their receptors have been implicated. During normal physiological function, the BGB may be remodeled in response to alterations in transmural pressures in both blood capillaries and airspaces. Such changes are mitigated through rapid expression of the relevant genes for extracellular matrix proteins and growth factors. While an appreciable amount of information regarding molecular control has been documented in the mammalian lung, very little is available on the avian lung.

Corrections to the Hazelhoff model of airflow in the avian lung

1979 ◽  
Vol 36 (2) ◽  
pp. 143-154 ◽  
Author(s):  
John Brackenbury
Keyword(s):  
Avian Lung

Gas-blood CO2 equilibration in parabronchial lungs of birds

1976 ◽  
Vol 41 (3) ◽  
pp. 302-309 ◽  
Author(s):  
M. Meyer ◽  
H. Worth ◽  
P. Scheid
Keyword(s):  
Steady State ◽  
Venous Blood ◽  
Blood Perfusion ◽  
Co2 Exchange ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Mixed Venous ◽  
Haldane Effect

We have conducted two experimental series in the chicken in order to study CO2 exchange in the parabronchial lungs of birds.In the first series, the animals were artifically ventilated and end-expired PCO2, PE'CO2,was measured and compared with mixed venous PCO2, PVCO2. On the average, PECO2 exceeded PVCO2 by 2.8 Torr. In the second series, rebreathing was used to investigate the mechanism of this positive (PE'-PV)CO2 difference.Lung gas PCO2 was found to equilibrate with PVCO2 if both CO2 and O2 exchange in the lung was abolished during rebreathing. Only if O2 uptake continued, we observed a positive gas-to-mixed venous blood PCO2 difference. The results suggest that positive gas-blood PCO2 differences both during rebreathing and steady-state ventilation are brought about by the Haldane effect.Model calculations show that in the homogeneous avian lung, unlike in the alveolar lung, the Haldane effect can produce positive (PE'-PV)CO2 differences during steady-state breathing due to the peculiarities of the crosscurrent arrangement and parabronchial ventilation and blood perfusion.

Accelerating and Retarding Effects of Dexamethasone on the Development of the Avian Lung

1989 ◽  
Vol 12 (3) ◽  
pp. 153-161 ◽  
Author(s):  
J. Wittmann ◽  
A. Steib ◽  
H.G. Liebich ◽  
P. Schmidt
Keyword(s):  
Avian Lung

Modulation of Avian Lung Eicosanoids by Dietary Omega-3 Fatty Acids

1987 ◽  
Vol 117 (7) ◽  
pp. 1197-1206 ◽  
Author(s):  
Margaret C. Craig-Schmidt ◽  
Sam A. Faircloth ◽  
John D. Weete
Keyword(s):  
Fatty Acids ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Avian Lung

Gas-blood PCO2 gradients during avian gas exchange

1975 ◽  
Vol 39 (3) ◽  
pp. 405-410 ◽  
Author(s):  
D. G. Davies ◽  
R. E. Dutton
Keyword(s):  
Gas Exchange ◽  
Exchange System ◽  
Arterial Pco2 ◽  
Charged Membrane ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Gas Exchange System ◽  
Spontaneously Breathing ◽  
Membrane Mechanism ◽  
Mixed Venous

The avian respiratory system is a crosscurrent gas exchange system. One of the aspects of this type of gas exchange system is that end-expired PCO2 is greater than arterial PCO2, the highest possible value being equal to mixed venous PCO2. We made steady-state measurements of arterial, mixed venous, and end-expired PCO2 in anesthetized, spontaneously breathing chickens during inhalation of room air or 4–8% CO2. We found end-expired PCO2 to be higher than both arterial and mixed venous PCO2, the sign of the differences being such as to oppose passive diffusion. The observation that end-expired PCO2 was higher than arterial PCO2 can be explained on the basis of crosscurrent gas exchange. However, the observation that end-expired PCO2 exceeded mixed venous PCO2 must be accounted for by some other mechanism. The positive end-expired to mixed venous PCO2 gradients can be explained if it is postulated that the charged membrane mechanism suggested by Gurtner et al. (Respiration Physiol. 7: 173–187, 1969) is present in the avian lung.

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