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.

Morphometry of the extremely thin pulmonary blood-gas barrier in the chicken lung

2007 ◽  
Vol 292 (3) ◽  
pp. L769-L777 ◽  
Author(s):  
Rebecca R. Watson ◽  
Zhenxing Fu ◽  
John B. West
Keyword(s):  
Type I Collagen ◽  
Arithmetic Mean ◽  
Type I ◽  
Blood Gas ◽  
Gas Barrier ◽  
Structural Support ◽  
Pulmonary Capillaries ◽  
Mammalian Lung ◽  
Avian Lung ◽  
To Come

The gas exchanging region in the avian lung, although proportionally smaller than that of the mammalian lung, efficiently manages respiration to meet the high energetic requirements of flapping flight. Gas exchange in the bird lung is enhanced, in part, by an extremely thin blood-gas barrier (BGB). We measured the arithmetic mean thickness of the different components (endothelium, interstitium, and epithelium) of the BGB in the domestic chicken lung and compared the results with three mammals. Morphometric analysis showed that the total BGB of the chicken lung was significantly thinner than that of the rabbit, dog, and horse (54, 66, and 70% thinner, respectively) and that all layers of the BGB were significantly thinner in the chicken compared with the mammals. The interstitial layer was strikingly thin in the chicken lung (∼86% thinner than the dog and horse, and 75% thinner than rabbit) which is a paradox because the strength of the BGB is believed to come from the interstitium. In addition, the thickness of the interstitium was remarkably uniform, unlike the mammalian interstitium. The uniformity of the interstitial layer in the chicken is attributable to a lack of the supportive type I collagen cable that is found in mammalian alveolar lungs. We propose that the surrounding air capillaries provide additional structural support for the pulmonary capillaries in the bird lung, thus allowing the barrier to be both very thin and extremely uniform. The net result is to improve gas exchanging efficiency.

scholarly journals Immuno-localization of type-IV collagen in the blood-gas barrier and the epithelial–epithelial cell connections of the avian lung

2013 ◽  
Vol 9 (1) ◽  
pp. 20120951 ◽  
Author(s):  
S. A. Jimoh ◽  
J. N. Maina
Keyword(s):  
Epithelial Cell ◽  
Type Iv Collagen ◽  
Basement Membranes ◽  
Blood Gas ◽  
Gas Barrier ◽  
Blood Capillaries ◽  
Mechanical Feature ◽  
Type Iv ◽  
Mammalian Lung ◽  
Avian Lung

The terminal respiratory units of the gas exchange tissue of the avian lung, the air capillaries (ACs) and the blood capillaries (BCs), are small and rigid: the basis of this mechanical feature has been highly contentious. Because the strength of the blood-gas barrier (BGB) of the mammalian lung has been attributed to the presence of type-IV collagen (T-IVc), localization of T-IVc in the basement membranes (BM) of the BGB and the epithelial–epithelial cell connections (E-ECCs) of the exchange tissue of the lung of the avian (chicken) lung was performed in order to determine whether it may likewise contribute to the strength of the BGB. T-IVc was localized in both the BM and the E-ECCs. As part of an integrated fibroskeletal scaffold on the lung, T-IVc may directly contribute to the strengths of the ACs and the BCs.

scholarly journals Mechanical ventilation-induced alterations of intracellular surfactant pool and blood–gas barrier in healthy and pre-injured lungs

2020 ◽  
Author(s):  
Jeanne-Marie Krischer ◽  
Karolin Albert ◽  
Alexander Pfaffenroth ◽  
Elena Lopez-Rodriguez ◽  
Clemens Ruppert ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Blood Gas ◽  
Control Groups ◽  
Gas Barrier ◽  
Alveolar Epithelial ◽  
Alveolar Surfactant ◽  
Healthy Control ◽  
Mean Size ◽  
The Mean ◽  
Injury Progression

AbstractMechanical ventilation triggers the manifestation of lung injury and pre-injured lungs are more susceptible. Ventilation-induced abnormalities of alveolar surfactant are involved in injury progression. The effects of mechanical ventilation on the surfactant system might be different in healthy compared to pre-injured lungs. In the present study, we investigated the effects of different positive end-expiratory pressure (PEEP) ventilations on the structure of the blood–gas barrier, the ultrastructure of alveolar epithelial type II (AE2) cells and the intracellular surfactant pool (= lamellar bodies, LB). Rats were randomized into bleomycin-pre-injured or healthy control groups. One day later, rats were either not ventilated, or ventilated with PEEP = 1 or 5 cmH2O and a tidal volume of 10 ml/kg bodyweight for 3 h. Left lungs were subjected to design-based stereology, right lungs to measurements of surfactant proteins (SP−) B and C expression. In pre-injured lungs without ventilation, the expression of SP-C was reduced by bleomycin; while, there were fewer and larger LB compared to healthy lungs. PEEP = 1 cmH2O ventilation of bleomycin-injured lungs was linked with the thickest blood–gas barrier due to increased septal interstitial volumes. In healthy lungs, increasing PEEP levels reduced mean AE2 cell size and volume of LB per AE2 cell; while in pre-injured lungs, volumes of AE2 cells and LB per cell remained stable across PEEPs. Instead, in pre-injured lungs, increasing PEEP levels increased the number and decreased the mean size of LB. In conclusion, mechanical ventilation-induced alterations in LB ultrastructure differ between healthy and pre-injured lungs. PEEP = 1 cmH2O but not PEEP = 5 cmH2O ventilation aggravated septal interstitial abnormalities after bleomycin challenge.

scholarly journals Targeting Selectins Mediated Biological Activities With Multivalent Probes

2021 ◽  
Vol 9 ◽  
Author(s):  
Deepak Ganesh ◽  
Prashant Jain ◽  
Chethan Devanur Shanthamurthy ◽  
Suraj Toraskar ◽  
Raghavendra Kikkeri
Keyword(s):  
Tumor Metastasis ◽  
Inflammatory Diseases ◽  
Biological Activities ◽  
Type I ◽  
Blood Capillaries ◽  
Activated Platelets ◽  
Selectin Ligands ◽  
Different Types ◽  
Selectin Binding ◽  
Sialyl Lewisa

Selectins are type-I transmembrane glycoproteins that are ubiquitously expressed on activated platelets, endothelial cells, and leukocytes. They bind to cell surface glycoproteins and extracellular matrix ligands, regulate the rolling of leukocytes in the blood capillaries, and recruit them to inflammatory sites. Hence, they are potential markers for the early detection and inhibition of inflammatory diseases, thrombosis, cardiovascular disorders, and tumor metastasis. Fucosylated and sialylated glycans, such as sialyl Lewisx, its isoform sialyl Lewisa, and heparan sulfate, are primary selectin ligands. Functionalization of these selectin-binding ligands on multivalent probes, such as nanoparticles, liposomes, and polymers, not only inhibits selectin-mediated biological activity but is also involved in direct imaging of the inflammation site. This review briefly summarizes the selectin-mediated various diseases such as thrombosis, cancer and recent progress in the different types of multivalent probes used to target selectins.

Roles of intra- and extracellular carbonic anhydrase in alveolar-capillary CO2 equilibration

1994 ◽  
Vol 77 (2) ◽  
pp. 697-705 ◽  
Author(s):  
T. A. Heming ◽  
E. K. Stabenau ◽  
C. G. Vanoye ◽  
H. Moghadasi ◽  
A. Bidani
Keyword(s):  
Carbonic Anhydrase ◽  
Driving Forces ◽  
Excretion Rate ◽  
Blood Gas ◽  
Gas Barrier ◽  
Arterial Pco2 ◽  
Co2 Diffusion ◽  
Chemical Equilibration ◽  
Co2 Excretion ◽  
Alveolar Capillary

Alveolar-capillary CO2 equilibration involves diffusive equilibration of CO2 across the blood-gas barrier and chemical equilibration of perfusate CO2-HCO-3-H+ reactions. These processes are governed by different, but related, driving forces and conductances. The present study examined the importance of pulmonary carbonic anhydrase (CA) for diffusive and reactive CO2 equilibration in isolated rat lungs. Lungs were perfused with salines containing membrane-impermeant or -permeant inhibitors of CA. Measurements of CO2 excretion rate, equilibrated venous and arterial PCO2 and pH, and postcapillary pH and PCO2 disequilibria were used, together with our previous model of CO2-HCO-3-H+ reactions and transport in saline-perfused capillaries (Bidani et al. J. Appl. Physiol. 55: 75–83, 1983), to compute the relevant driving forces and conductances. Reactive CO2 equilibration was markedly affected by extracellular (vascular) CA activity but not by the activity of intracellular (cytosolic) CA. The driving force for CO2 diffusion was strongly influenced by vascular CA activity. The conductance for CO2 diffusion was independent of CA activity. The minimum conductance for CO2 diffusion was estimated to be 700–800 ml.min-1.Torr-1. The results indicate that extracellular vascular CA activity influences both diffusive and reactive CO2 equilibration. However, cytosolic CA has no detectable role in alveolar-capillary CO2 equilibration.

Diffusion characteristics of pulmonary blood-gas barrier at low temperatures.

1971 ◽  
Vol 31 (3) ◽  
pp. 438-446 ◽  
Author(s):  
G G Power ◽  
V S Aoki ◽  
W H Lawson ◽  
J B Gregg
Keyword(s):  
Low Temperatures ◽  
Blood Gas ◽  
Gas Barrier ◽  
Diffusion Characteristics

Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs

1975 ◽  
Vol 38 (6) ◽  
pp. 1099-1109 ◽  
Author(s):  
P. D. Wagner ◽  
R. B. Laravuso ◽  
E. Goldzimmer ◽  
P. F. Naumann ◽  
J. B. West
Keyword(s):  
Pulmonary Embolism ◽  
Steady State ◽  
Gas Exchange ◽  
Clinical Investigation ◽  
Inert Gas ◽  
Blood Gas ◽  
Gas Barrier ◽  
Initial Application ◽  
Arterial Po2 ◽  
Made In

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.

New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay

2019 ◽  
Vol 25 (3) ◽  
pp. 769-785 ◽  
Author(s):  
Doaa M. Mokhtar ◽  
Manal T. Hussein ◽  
Marwa M. Hussein ◽  
Enas A. Abd-Elhafez ◽  
Gamal Kamel
Keyword(s):  
Tunel Assay ◽  
Second Phase ◽  
Type I ◽  
Apoptotic Cells ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Blood Capillaries ◽  
Pulmonary Alveoli ◽  
Alveolar Septa ◽  
Terminal Bronchiole

AbstractThis study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood–air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air–blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air–blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air–blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.

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