Academic literature on the topic 'Alveolar air'
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Journal articles on the topic "Alveolar air"
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Wang, P. M., Y. Ashino, H. Ichimura, and J. Bhattacharya. "Rapid alveolar liquid removal by a novel convective mechanism." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 6 (December 1, 2001): L1327—L1334. http://dx.doi.org/10.1152/ajplung.2001.281.6.l1327.
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Although alveoli clear liquid by active transport, the presence of surface-active material on the alveolar surface suggests that convective mechanisms for rapid liquid removal may exist. To determine such mechanisms, we held the isolated blood-perfused rat lung at a constant alveolar pressure (Pa). Under videomicroscopy, we micropunctured a single alveolus to infuse saline or Ringer solution in ∼10 adjacent alveoli. Infused alveoli were lost from view. However, as the infused liquid cleared, the alveoli reappeared and their diameters could be quantified. Hence the time-dependent determination of alveolar diameter provided a means for quantifying the time to complete liquid removal (C t ) in single alveoli. All determinations were obtained at an Pa of 5 cmH2O. C t , which related inversely to alveolar diameter, averaged 4.5 s in alveoli with the fastest liquid removal. Injections of dye-stained liquid revealed that the liquid flowed from the injected alveoli to adjacent air-filled alveoli. Lung hyperinflations instituted by cycling Pa between 5 and 15 cmH2O decreased C t by 50%. Chelation of intracellular Ca2+ prolonged C t and abolished the inflation-induced enhancement of liquid removal. We conclude that when liquid is injected in a few alveoli, it rapidly flows to adjacent air-filled alveoli. The removal mechanisms are dependent on alveolar size, inflation, and intracellular Ca2+. We speculate that removal of liquid from the alveolar surface is determined by the curvature and surface-active properties of the air-liquid interface.
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Nunn, John F. "Alveolar Air Equations." Anesthesiology 85, no. 4 (October 1, 1996): 940. http://dx.doi.org/10.1097/00000542-199610000-00035.
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Nielson, D. W., and M. B. Lewis. "Effects of amiloride on alveolar epithelial PD and fluid composition in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 4 (April 1, 1990): L215—L219. http://dx.doi.org/10.1152/ajplung.1990.258.4.l215.
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To look for evidence of active absorption of Na+ in the alveolus in vivo in air-filled lungs, we measured [K+] and [Cl-] in the alveolar lining fluid and the potential difference (PD) across the alveolar epithelium by puncturing alveoli in lungs of anesthetized rabbits with nonselective and ion-selective microelectrodes. After intravenous doses of amiloride, the PD and [K+] decreased (-1.0 +/- 0.3 to -0.3 +/- 0.1 mV, 7.4 +/- 1.1 to 4.2 +/- 0.4 meq/l, P less than 0.001), but [Cl-] did not change (96 +/- 9, 94 +/- 4 meq/l). In another set of experiments, the PD was measured with microelectrodes filled with an electrolyte solution, and midway through each measurement some of the solution was injected into the alveolar lumen. Injecting the solution without amiloride did not alter the alveolar PD (-1.0 +/- 0.4 before and -1.1 +/- 0.5 after injection). The alveolar PD decreased to -0.1 +/- 0.2 mV after injecting the solution with 10(-5) M amiloride into the alveolar interior. These results support the hypothesis that alveolar epithelium in air-filled lungs actively absorbs sodium in vivo, which accounts for the majority of the transepithelial PD.
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Chen, Zheng-long, Ya-zhu Chen, and Zhao-yan Hu. "A micromechanical model for estimating alveolar wall strain in mechanically ventilated edematous lungs." Journal of Applied Physiology 117, no. 6 (September 15, 2014): 586–92. http://dx.doi.org/10.1152/japplphysiol.00072.2014.
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To elucidate the micromechanics of pulmonary edema has been a significant medical concern, which is beneficial to better guide ventilator settings in clinical practice. In this paper, we present an adjoining two-alveoli model to quantitatively estimate strain and stress of alveolar walls in mechanically ventilated edematous lungs. The model takes into account the geometry of the alveolus, the effect of surface tension, the length-tension properties of parenchyma tissue, and the change in thickness of the alveolar wall. On the one hand, our model supports experimental findings (Perlman CE, Lederer DJ, Bhattacharya J. Am J Respir Cell Mol Biol 44: 34–39, 2011) that the presence of a liquid-filled alveolus protrudes into the neighboring air-filled alveolus with the shared septal strain amounting to a maximum value of 1.374 (corresponding to the maximum stress of 5.12 kPa) even at functional residual capacity; on the other hand, it further shows that the pattern of alveolar expansion appears heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. The proposed model is a preliminary step toward picturing a global topographical distribution of stress and strain on the scale of the lung as a whole to prevent ventilator-induced lung injury.
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Raj, J. U., R. L. Conhaim, and J. Bhattacharya. "Micropuncture measurement of alveolar liquid pressure in excised dog lung lobes." Journal of Applied Physiology 62, no. 2 (February 1, 1987): 781–84. http://dx.doi.org/10.1152/jappl.1987.62.2.781.
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We have investigated the mechanism of alveolar liquid filling in pulmonary edema. We excised, degassed, and intrabronchially filled 14 dog lung lobes from nine dogs with 75, 150, 225, or 350 ml of 5% albumin solution, and then air inflated the lobes to a constant airway pressure of 25 cmH2O. By use of micropipettes, we punctured subpleural alveoli to measure alveolar liquid pressure by the servo-null technique. Alveolar liquid pressure was constant in all lobes despite differences in lobe liquid volume and averaged 10.6 +/- 1.3 cmH2O. Thus, in all lobes a constant pressure drop of 14.4 cmH2O existed from airway to alveolar liquid across the air-liquid interface. We attribute this finding, on the basis of the Laplace equation, to an air-liquid interface of constant radius in all the lobes. In fact, we calculated from the Laplace equation an air-liquid interface radius which equalled morphological estimates of alveolar radius. We conclude that in the steady state, alveoli that contained liquid have a constant radius of curvature of the air-liquid interface possibly because they are always completely liquid filled.
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Conhaim, R. L. "Airway level at which edema liquid enters the air space of isolated dog lungs." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2234–42. http://dx.doi.org/10.1152/jappl.1989.67.6.2234.
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To identify lung units associated with liquid leakage into the air space in high-pressure pulmonary edema, we perfused air-inflated dog lung lobes with albumin solution to fill the loose peribronchovascular interstitium. Next, we perfused the lobes for 90 s with fluorescent albumin solution then froze the lobes in liquid nitrogen. This procedure confined the fluorescent perfusate to the liquid flux pathway between the circulation and the air space and eliminated the previously filled peribronchovascular cuffs as a source of the fluorescence that entered the air space. We divided each frozen lobe into three horizontal layers and prepared fluorescence-microscopic sections of each layer. In the most apical layers where alveolar flooding was minimal, 10.6 +/- 21.0% (SD) of alveolar ducts were either fluorescence filled or air filled and continuous with fluorescence-filled alveoli. In the same layers, 11.0 +/- 19.0% of respiratory bronchioles were similarly labeled. No terminal bronchioles in these layers were fluorescence labeled. This suggested that the fluorescent albumin entered the air space across the epithelium of respiratory bronchioles, alveolar ducts, or their associated alveoli. To simulate an alternative explanation, i.e., that fluorescence first entered central airways then flowed into peripheral air spaces, we prepared two additional lobes that we first partially inflated with fluorescent albumin then filled to capacity with air. This pushed the fluorescent solution along the airways into the lung periphery. In these lobes the ciliary lining of bronchi and terminal bronchioles was fluorescence coated. By comparison, cilia in fluorescence-perfused lobes were not coated. We conclude that alveolar flooding in hydrostatic pulmonary edema occurs across the epithelium of alveolar ducts, respiratory bronchioles, or their associated alveoli.(ABSTRACT TRUNCATED AT 250 WORDS)
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Ochs, Matthias, Jan Hegermann, Elena Lopez-Rodriguez, Sara Timm, Geraldine Nouailles, Jasmin Matuszak, Szandor Simmons, Martin Witzenrath, and Wolfgang M. Kuebler. "On Top of the Alveolar Epithelium: Surfactant and the Glycocalyx." International Journal of Molecular Sciences 21, no. 9 (April 27, 2020): 3075. http://dx.doi.org/10.3390/ijms21093075.
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Gas exchange in the lung takes place via the air-blood barrier in the septal walls of alveoli. The tissue elements that oxygen molecules have to cross are the alveolar epithelium, the interstitium and the capillary endothelium. The epithelium that lines the alveolar surface is covered by a thin and continuous liquid lining layer. Pulmonary surfactant acts at this air-liquid interface. By virtue of its biophysical and immunomodulatory functions, surfactant keeps alveoli open, dry and clean. What needs to be added to this picture is the glycocalyx of the alveolar epithelium. Here, we briefly review what is known about this glycocalyx and how it can be visualized using electron microscopy. The application of colloidal thorium dioxide as a staining agent reveals differences in the staining pattern between type I and type II alveolar epithelial cells and shows close associations of the glycocalyx with intraalveolar surfactant subtypes such as tubular myelin. These morphological findings indicate that specific spatial interactions between components of the surfactant system and those of the alveolar epithelial glycocalyx exist which may contribute to the maintenance of alveolar homeostasis, in particular to alveolar micromechanics, to the functional integrity of the air-blood barrier, to the regulation of the thickness and viscosity of the alveolar lining layer, and to the defence against inhaled pathogens. Exploring the alveolar epithelial glycocalyx in conjunction with the surfactant system opens novel physiological perspectives of potential clinical relevance for future research.
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van den Velde, Sandra, Marc Quirynen, Paul van Hee, and Daniel van Steenberghe. "Differences between Alveolar Air and Mouth Air." Analytical Chemistry 79, no. 9 (May 2007): 3425–29. http://dx.doi.org/10.1021/ac062009a.
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Porzionato, Andrea, Diego Guidolin, Veronica Macchi, Gloria Sarasin, Davide Grisafi, Cinzia Tortorella, Arben Dedja, Patrizia Zaramella, and Raffaele De Caro. "Fractal analysis of alveolarization in hyperoxia-induced rat models of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 7 (April 1, 2016): L680—L688. http://dx.doi.org/10.1152/ajplung.00231.2015.
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No papers are available about potentiality of fractal analysis in quantitative assessment of alveolarization in bronchopulmonary dysplasia (BPD). Thus, we here performed a comparative analysis between fractal [fractal dimension ( D) and lacunarity] and stereological [mean linear intercept ( Lm), total volume of alveolar air spaces, total number of alveoli, mean alveolar volume, total volume and surface area of alveolar septa, and mean alveolar septal thickness] parameters in experimental hyperoxia-induced models of BPD. At birth, rats were distributed between the following groups: 1) rats raised in ambient air for 2 wk; 2) rats exposed to 60% oxygen for 2 wk; 3) rats raised in normoxia for 6 wk; and 4) rats exposed to 60% hyperoxia for 2 wk and to room air for further 4 wk. Normoxic 6-wk rats showed increased D and decreased lacunarity with respect to normoxic 2-wk rats, together with changes in all stereological parameters except for mean alveolar volume. Hyperoxia-exposed 2-wk rats showed significant changes only in total number of alveoli, mean alveolar volume, and lacunarity with respect to equal-in-age normoxic rats. In the comparison between 6-wk rats, the hyperoxia-exposed group showed decreased D and increased lacunarity, together with changes in all stereological parameters except for septal thickness. Analysis of receiver operating characteristic curves showed a comparable discriminatory power of D, lacunarity, and total number of alveoli; Lmand mean alveolar volume were less discriminative. D and lacunarity did not show significant changes when different segmentation thresholds were applied, suggesting that the fractal approach may be fit to automatic image analysis.
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Denny, E., and R. C. Schroter. "The Mechanical Behavior of a Mammalian Lung Alveolar Duct Model." Journal of Biomechanical Engineering 117, no. 3 (August 1, 1995): 254–61. http://dx.doi.org/10.1115/1.2794178.
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A model for the mechanical properties of an alveolar duct is analyzed using the finite element method. Its geometry comprises an assemblage of truncated octahedral alveoli surrounding a longitudinal air duct. The amounts and distributions of elastin and collagen fiber bundles, modeled by separate stress-strain laws, are based upon published data for dogs. The surface tension of the air-liquid interface is modeled using an area-dependent relationship. Pressure-volume curves are computed that compare well with experimental data for both saline-filled and air-filled lungs. Pressure-volume curves of the separate elastin and collagen fiber contributions are similar in form to the behavior of saline-filled lungs treated with either elastase or collagenase. A comparison with our earlier model, based upon a single alveolus, shows the duct to have a behavior closer to reported experimental data.
Dissertations / Theses on the topic "Alveolar air"
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Anderson, Lynda Grace. "Investigation of alveolar epithelial cell synthesis of fibrinogen in response to particulate air pollution." Thesis, Edinburgh Napier University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270652.
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Schruf, Eva [Verfasser]. "Recapitulating aspects of alveolar epithelial dysfunction related to idiopathic pulmonary fibrosis utilizing an iPSC-derived air-liquid interface model system / Eva Schruf." Ulm : Universität Ulm, 2020. http://d-nb.info/1219964794/34.
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Lima, Marcos Pereira. "Equações preditivas para determinar a temperatura interna do ar: envolventes em painel alveolar com cobertura verde." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/18/18139/tde-03122009-160414/.
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Introdução: Através da ferramenta estatística denominada análise de regressão linear múltipla se gerou equações preditivas de temperatura interna do ar de uma edificação com paredes e lajes compostas por painéis de concreto alveolar, com sistema de cobertura verde. Justificativa: Com equações preditivas é possível simular temperaturas internas de edificações utilizando uma pequena entrada de dados com uma precisão satisfatória. Utilizando tais equações é possível, também, corrigir erros de projetos antes de sua execução. Objetivos: Gerar equações preditivas para o período seco (outono e inverno) e para o período chuvoso (primavera e verão) para a edificação analisada. Metodologia: Foram selecionadas duas séries de dados, um referente ao período de característica seca e outro de característica chuvosa. Foram geradas equações preditivas de temperatura interna do ar máxima, média e mínima para os dois períodos, utilizando análise de regressão linear. Resultados: Foram geradas sete equações preditivas para o período seco e cinco para o período chuvoso. As diferenças máximas, em módulo, entre as temperaturas estimadas pelas equações e as monitoradas experimentalmente ficaram em aproximadamente 2°C. Conclusão: As equações preditivas geradas para os dois períodos considerados descrevem satisfatoriamente o comportamento térmico da edificação.Introduction: Using a statistics tool called multiple linear regression, we created equations for predicting the indoor temperature in a building with walls and ceiling build from panels of alveolar concrete, with a green roof system. Explanation: Predictive equations enable simulations of indoor temperatures of buildings using a small number of data and with a satisfactory precision. They also allow corrections on project errors before they are put into effect. Objectives: Generate predictive equations for the building for the dry season (autumn and winter) and for the rainy season (spring and summer). Method: We selected two series of data, one for the dry and one for the rainy season. Using linear regression analysis we ran predictive equations for maximum, intermediate and minimum indoor temperatures of the air for both seasons. Results: We created seven predictive equations for the dry season and five for the wet season. The largest differences (in module) between the temperatures estimated using equations and monitored experimentally was approximately 2°C. Conclusion: The predictive equations generated for both periods described satisfactorily the thermal behavior of the building.
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Padovan, Michele Galhardoni. "Material particulado de carbono nos compartimentos de tecidos de macrófagos alveolares e de superfície pulmonar de residentes de São Paulo, Brasil." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-20062017-113703/.
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Introdução Os fumantes inalam grandes quantidades de partículas de carbono, o que pode contribuir para efeitos adversos pulmonares e sistêmicos. É sabido que os macrófagos alveolares (MA) desempenham um papel extremamente importante no reconhecimento e processamento de qualquer material estranho inalado e são as células predominantes que processam e removem partículas inaladas. Existe também a deposição superficial a longo prazo do carbono observado nos pulmões de fumantes em autópsias. Atualmente, a distribuição e retenção de partículas de fumo derivadas de cigarros quando a pessoa também está exposta a níveis elevados de poluição do ar ainda não é clara. Portanto, procurou-se avaliar a carga de carbono nos MA e a deposição de superfície pulmonar em uma população exposta a alta poluição atmosférica (São Paulo), tanto em fumantes como não-fumantes. Métodos Uma coorte de 72 sujeitos post mortem foi obtida do Serviço de Verificação de Óbitos da Capital da Universidade de São Paulo (SVOC). As imagens das superfícies pulmonares foram obtidas sob condições padrão e pequenos fragmentos de tecido pulmonar foram coletados para análise de macrófagos usando a técnica de esfregaço. A superfície total de negro de carbono foi analisada utilizando o programa Imagem J (National Institute of Health, MD, EUA), teste cego ao fumo. A absorção interna de carbono nos MA foi medida utilizando o programa Image Pro Plus (The Proven Solution, Media Cybernetics Inc., EUA). A aprovação ética foi obtida. A média de negro de carbono de macrófagos tanto em fumantes como em não-fumantes foi analisada utilizando teste de Mann Whitney e expressa como intervalo interquartil (IQR). Resultados Os fumantes têm um nível significativamente mais elevado de negro de carbono nos macrófagos alveolares (103.4 (IQR 29.44 to 226.3) vs. 9.27 (IQR 3.1 to 85.13) um2, P < 0.001)103.4um2. Não houve diferença significativa entre a área média de deposição superficial de carbono nos pulmões de fumantes e não fumantes de 6, 74 cm2 (IQR 3, 47 a 10, 02) versus 5, 20 cm2 (IQR 2, 29 a 7, 54) P=NS. Conclusão O teor de carbono nos MA é claramente muito maior nos fumantes do que os nãofumantes. No entanto, a análise da superfície pulmonar não mostrou diferença significativa. Isso pode indicar que, em uma área de alta poluição do ar, o principal fator que contribui para a deposição de carbono no pulmão a longo prazo é a exposição à poluição com efeitos limitados da exposição à fumaça de cigarro. O preto de carbono nos MA ainda aparece significativamente influenciado pela exposição à fumaça de cigarroRationale Smokers inhale large amounts of carbonaceous particulate matter, which may contribute to pulmonary and systemic adverse effects. It is clear that alveolar macrophages (AM) play a critically important role in the recognition and processing of any inhaled foreign material and are the predominant cells that process and remove inhaled particulate matter from the lung. There is also long-term surface deposition of carbon seen in the lungs of smokers at post-mortem. At present the distribution and retention of cigarette smoke-derived particulate matter when the person is also exposed to high levels of background air pollution is unclear. Therefore we sought to assess both AM carbon loading and lung surface deposition in a population exposed to high background air pollution (São Paulo) in both smokers and non-smokers. Methods A cohort of 72 post-mortem subjects was obtained from São Paulo Autopsy Centre (SVOC). Images of lung surfaces were obtained under standard conditions and small fragments of lung tissue were collected for macrophage analysis using smear technique. The total surface black carbon was analysed using Image J (National Institute of Health, MD, USA), blinded to smoking status. Internal AM carbon uptake was measured using Image Pro Plus (The Proven Solution, Media Cybernetics Inc., USA). Ethical approval was obtained. Mean macrophage black carbon in both smokers and non-smokers was analysed using Mann Whitney and expressed as median (IQR). Results Smokers have a significantly higher level of mean macrophage black carbon (103.4 (IQR 29.44 to 226.3) vs. 9.27 (IQR 3.1 to 85.13) um2, P < 0.001)103.4um2. There was no significant difference between the mean area of surface deposition of carbon in the lungs of smokers and non-smokers 6.74 cm2 (IQR 3.47 to 10.02) versus 5.20cm2 (IQR 2.29 to 7.54) P=NS. Conclusion AM carbon content is clearly much higher in the smokers than the non-smokers. However the lung surface analysis showed no significant difference. This could indicate that in an area of high air pollution the main contributing factor to long term lung carbon deposition is pollution exposure with limited effects from cigarette smoke exposure. AM black carbon still appears significantly influenced by cigarette smoke exposure
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Kühn, Anna Michele [Verfasser], and Claus-Michael [Akademischer Betreuer] Lehr. "Immortalization of human alveolar epithelial cells : towards a cell line expressing functional tight junctions for modelling the air-blood barrier in vitro / Anna Michele Kühn. Betreuer: Claus-Michael Lehr." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/110979021X/34.
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Masson, Romain. "Matériaux photocatalytiques structurés à base de mousses alvéolaires de β-SiC : applications au traitement de l'air." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00836563.
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L'objectif principal de ce travail a été d'étudier le potentiel de mousses alvéolaires tridimensionnelles en carbure de silicium de forme béta (β-SiC) comme support de photocatalyseur, dans le but de mettre au point des réacteurs photocatalytiques structurés pour le traitement de l'air. Ces mousses alvéolaires de β-SiC de surface spécifique moyenne et de porosité très ouverte sont obtenues par la synthèse dite à mémoire de forme (Shape Memory Synthesis), consistant en la carburation contrôlée d'une mousse alvéolaire de polyuréthane préformée. Une étude de la dégradation de trois polluants sur des films minces en mode de lit léchant (la méthyléthylcétone, l'ammoniac et le sulfure d'hydrogène) a tout d'abord permis de sélectionner trois photocatalyseurs d'intérêt parmi six références commerciales avant d'être immobilisés sur les mousses de β-SiC. Après une étape d'optimisation en termes de taille d'alvéoles, de nature et quantité de photocatalyseur, le média photocatalytique TiO2/mousses de β-SiC a été caractérisé et ses performances comparées en mode mono-passage ainsi qu'en mode de recirculation du flux dans une enceinte de 2 m3, à celles d'un film mince de TiO2 et d'un média photocatalytique commercial de référence. Le média photocatalytique TiO2/mousses de β-SiC présente des performances nettement améliorées par rapport à celles du média référent. Les mousses jouent un rôle de mélangeur statique et permettent une meilleure utilisation du volume du réacteur, en augmentation la densité de photocatalyseur par unité de volume tout en maintenant une illumination du cœur du réacteur acceptable ainsi que des pertes de charge très limitées.
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Fougère, Bertrand. "Influence de l'âge et du tabac sur les mécanismes génotoxiques et épigénétiques précoces de cancérogénèse broncho-pulmonaire en réponse à la pollution particulaire urbaine." Thesis, Littoral, 2014. http://www.theses.fr/2014DUNK0377/document.
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Récemment reconnus comme cancérogènes certains pour l'homme par l’IARC, la pollution atmosphérique et les particules fines (PM₂.₅) peuvent être inhalées et pourraient être retenues au niveau pulmonaire ou passer dans la circulation systémique. Ceci peut causer ou renforcer de nombreuses pathologies auxquelles les personnes âgées sont souvent plus sensibles. Cette thèse s’inscrit dans une démarche d’identification des processus impliqués dans la modulation du potentiel cancérogène des PM₂.₅, en lien avec l’âge ou le statut tabagique. Les particules ont été collectées à Dunkerque, agglomération présentant des influences maritimes mais également caractérisée par des activités industrielles et un trafic automobile importants. Pour évaluer l'influence de l'âge, des lymphocytes sanguins prélevés chez 90 patients issus de trois classes d'âge (25-30, 50-55 et 75-80 ans) ont été exposés ex vivo à des PM₂.₅ d’origine urbaine. Les lymphocytes isolés ont été exposés aux PM₂.₅ pendant 72 heures, avant de mesurer l'activité télomérase et la modulation d'expression de gènes tels que P16INK4A et MGMT. Les PM₂.₅ entraînent des variations de l'activité télomérase et de la longueur des télomères dans toutes les tranches d'âge indifféremment. L’expression du gène P16INK4A est significativement augmentée avec l'âge après exposition aux PM₂.₅. L'âge augmenterait l'expression du gène MGMT après exposition aux particules, en diminuant le niveau de méthylation de son promoteur uniquement dans le groupe des patients les plus âgés. Concernant le rôle du statut tabagique, 26 lavages broncho-alvéolaires ont été réalisés chez des patients fumeurs et non-fumeurs. Les macrophages issus de ces prélèvements ont été mis en culture avec des cellules épithéliales bronchiques BEAS-2B, avant exposition aux PM₂.₅ (3 et 15 µg/cm², 72 h). L’activité télomérase et la longueur des télomères varient après exposition aux PM2.5 et le statut tabagique modifie ces paramètres dans les cellules BEAS-2B et les macrophages alvéolaires. La méthylation des promoteurs et l’expression des gènes P16INK4A et MGMT ne sont pas modifiées dans les cellules BEAS-2B, alors que dans les macrophages alvéolaires les particules induisent l’expression de ces gènes par une diminution de la méthylation de leurs promoteurs. Le statut tabagique fumeur semble au contraire accroître la méthylation et limite l’expression de ces deux gènes. En conclusion, il apparaît que l’échantillon de PM₂.₅ étudié peut induire ex vivo plusieurs lésions décrites dans les étapes d’initiation et de promotion de la cancérogenèse broncho-pulmonaire. L’âge et le tabagisme sont susceptibles de moduler les effets toxiques des particules. Alors que les symptômes du cancer du poumon apparaissent seulement à une étape avancée de la maladie, nos résultats pourraient aider à la découverte de nouveaux marqueurs de diagnostic précoce permettant ainsi d’améliorer la survieRecently recognized as carcinogenic to human by IARC, air pollution and fine particulate matter (PM₂.₅) can be inhaled and could be retained into the lung or reach the systemic circulation. This can cause or worsen many diseases for which the elderly are often more sensitive. The PhD objective corresponds to the identification of the mechanisms of action involved in the modulation of carcinogenic potential of PM₂.₅, in connection with age or smoking status. PM₂.₅ were collected in Dunkerque, a French seaside city characterized by important industrial activities and heavy motor vehicle traffic. In order to estimate the influence of age, blood lymphocytes sampled from 90 patients from age classes (25-30, 50-55 and 75-80 years old) were ex vivo exposed to PM₂.₅ during 72 hours, before evaluation of telomerase activity and gene expression modulation of P16INK4A and MGMT. PM₂.₅ modulated telomerase activity and telomeres length in all age groups without any influence of age. P16INK4A gene expression increased significantly with age after exposure to PM₂.₅. Age could enhance MGMT gene expression after exposure to particles by decreasing the level of promoter methylation in the oldest group. Regarding the role of smoking status, 26 broncho-alveolar lavage were performed in smoker and non-smoker people. Macrophages were cultured with bronchial epithelial BEAS-2B cells before PM₂.₅ exposure (3 or 15µg/cm²; 72h). The telomerase activity and telomere length vary after exposure and the tobacco modify these parameters in BEAS-2B cells and alveolar macrophages. Methylation of P16INK4A and MGMT genes promoters and their expression are not modified in BEAS-2B cells. In alveolar macrophages, particles lead to a decrease of methylation of P16INK4A gene promoter. The smoking status seems also to increase methylation and to down-regulate expression of these two genes. In conclusion, it seems that the studied PM₂.₅ sample can induce ex vivo modifications described in the initiation and promotion of lung carcinogenesis. The age and smoking status may modulate the toxic effects of particles. Since lung cancer symptoms appear only at an advanced stage, our results could help in proposing new biomarkers of carcinogenesis allowing an early diagnosis to improve survival
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TISATO, Silvia. "Detection of volatile organic compounds in the alveolar air of subjects with stress-related psychopathologies." Doctoral thesis, 2011. http://hdl.handle.net/11562/349138.
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Dosaggio dei composti organici volatili nell’aria alveolare di soggetti con psicopatologie stress-correlate
L’aumento della domanda lavorativa insieme a maggiori livelli di stress hanno effetti negative sulla salute dei lavoratori, compresa l’insorgenza di disturbi mentali. Lo stress è all’origine di diverse forme di disagio lavorativo tra cui il Mobbing, la Costrittività organizzativa e il Burn-out che a loro volta sono espressione di stress psicosociale. Molti studi includono tra le psicopatologie stress-correlate il disturbo misto ansioso-depressivo, il disturbo d’ansia e il disturbo depressivo. L’INAIL riconosce ed indennizza il Disturbo dell’Adattamento e il Disturbo Post-Traumatico da Stress come malattie professionali riconducibili a situazioni di Costrittività organizzativa. La fisiopatologia dello stress è nota da tempo e i biomarcatori attualmente utilizzati per la diagnosi dello stress, come il cortisolo in matrici biologiche quali sangue, urina e saliva si ottengono con metodi invasivi e protocolli complessi. Nell’ultimo decennio sono stati pubblicati molti studi che hanno documentato il possibile ruolo dell’aria alveolare nella diagnosi di diverse patologie (neoplastiche, metaboliche, infiammatorie) fornendo informazioni riguardo lo stato metabolico del paziente. Alcuni studi hanno applicato l’analisi dell’aria alveolare anche alle psicopatologie, in particolare la schizofrenia. 98 lavoratori con disturbi mentali e somatoformi correlati a condizioni di stress lavorativo cronico e 80 volontari sani sono stati sottoposti alla raccolta di campioni di aria alveolare. Sono state dosate le concentrazioni di circa cento composti organici volatili nell’espirio utilizzando l’analisi in spettrometria di massa – IMR. La maggior parte dei composti era nota solo per la massa. I dati sono stati analizzati mediante analisi statistica multivariata; si sono ottenuti due modelli che con una combinazione rispettivamente di undici molecole (pentano, ciclopentadiene, acetonitrile, butadiene, acido cianidrico, M70, M71, M74, M75, M97 E M123) e di tre molecole (M27, eptano e M 101) sono stati in grado distinguere i casi dai controlli sani con una sensibilità del 100% e una specificità del 98,75%. L’utilizzo della spettrometria di massa ha comportato numerosi vantaggi: innanzitutto il breve tempo richiesto per dosare circa cento molecole per ciascun campione e il costo contenuto grazie alla possibilità di dosare simultaneamente centinaia di campioni al giorno; inoltre l’elevata sensibilità ha permesso di quantificare molecole a concentrazioni bassissime (ppb: parti per bilione). Il prelievo di aria alveolare è semplice, non invasivo e l’analisi strumentale non è costosa. L’identificazione di uno o più profili di composti organici volatili elettivi nell’aria alveolare potrebbe essere utile nella diagnosi delle psicopatologie stress correlate.Detection of volatile organic compounds in the alveolar air of subjects with stress-related psychopathologies The upsurge of job demand together with more high-level of Stress, have negative effects on the health of workers including mental disorders. Stress is responsible for various forms of working uneasiness, among which Personal Bullying, Task-related Bullying and Burn-Out that are different expressions of psychosocial Stress. Manifold studies include Depression, Anxious and mixed Anxious-Depressive Disorders among the stress-related psychopathologies. The Italian Institute for Insurance against Industrial Accident (INAIL) recognizes and indemnifies the Post-Traumatic Stress Disorder (PTSD) and the Adjustment Disorder as professional illnesses referable to situations of Task-related Bullying. The physiopathology of stress has been known for many years and the biomarkers used for the diagnosis of stress such as cortisol in biological matrices like blood, urine and saliva are obtained with invasive methods and nonelementary protocols. In the last decade many studies have been published documenting the potential role of the alveolar air in the diagnosis of different pathologies (neoplastic, metabolic, inflammatory) through informations on the metabolic state of the patient. Some studies have also applied the analysis of the alveolar air to the psychopathologies, mainly to schizophrenia. 98 workers with mental and somatoform disorders correlated with situations of chronic stress at work and 80 healthy volunteers were submitted to the alveolar air sampling. Concentrations of about one hundred volatile compounds were measured in the exhaled breath using IMR - Mass Spectrometry. Most of the compounds were known only for their masses. A multivariate statistical analysis was performed. Using two different models with a combination respectively of eleven molecules (pentane, cyclopentadiene, acetonitrile, butadiene, hydrocyanic acid, M70, M71, M74, M75, M97 and M123) and three molecules (M27, heptane and M101) has been possible to distinguish the cases from the healthy controls with a 100% sensibility and a 98,75% specificity. The use of mass spectrometry has entailed different advantages: first of all the short time required for the dosing of about one hundred molecules in each sample and the low cost thanks to the possibility to simultaneously analyze hundreds of samples a day; besides the high sensibility of the mass spectrometry analysis allows to quantify molecules at very low concentrations (ppb). Alveolar air sampling is simple and non-invasive and the instrumental analysis is not expensive. The identification of one or more profiles of elective volatile organic compounds in the alveolar air would be useful in the diagnosis of stress-related psychopathologies.
Books on the topic "Alveolar air"
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Khan, Nayema, and John Pawlowski. Disruption of Diffusion. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0020.
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Adequate gas exchange in the lungs requires a balance between three key processes: ventilation (V), the flow of gas from the environment to the alveoli; perfusion (Q), the circulation to the pulmonary capillary beds; and diffusion of the gas from the alveolar space into the alveolar capillaries. This chapter discusses the management of diseases of the air space, which include secretions, pneumonia, pulmonary edema, and hemoptysis. Collectively these conditions result in the build-up of fluid in the alveolar space and thickening of the alveolar membrane, leading to a mismatch in ventilation and perfusion (V/Q mismatch). Both anesthesia and disease states can adversely affect gas exchange and the chapter discusses strategies to maximize a patient’s pulmonary status in order to minimize perioperative pulmonary complications.
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Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.
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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
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Martin-Loeches, Ignacio, and Antonio Artigas. Respiratory support with positive end-expiratory pressure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0094.
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Positive-end-expiratory pressure (PEEP) is the pressure present in the airway (alveolar pressure) above atmospheric pressure that exists at the end of expiration. The term PEEP is defined in two particular settings. Extrinsic PEEP (applied by ventilator) and intrinsic PEEP (PEEP caused by non-complete exhalation causing progressive air trapping). Applied (extrinsic) PEEP—is usually one of the first ventilator settings chosen when mechanical ventilation (MV) is initiated. Applying PEEP increases alveolar pressure and volume. The increased lung volume increases the surface area by reopening and stabilizing collapsed or unstable alveoli. PEEP therapy can be effective when used in patients with a diffuse lung disease with a decrease in functional residual capacity. Lung protection ventilation is an established strategy of management to reduce and avoid ventilator-induced lung injury and mortality. Levels of PEEP have been traditionally used from 5 to 12 cmH2O; however, higher levels of PEEP have also been proposed and updated in order to keep alveoli open, without the cyclical opening and closing of lung units (atelectrauma). The ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension; however, it should be individualized and higher PEEP might be used in the more severe end of the spectrum of patients with improved survival. A survival benefit for higher levels of PEEP has not been yet reported for any patient under MV, but a higher PaO2/FiO2 ratio seems to be better in the higher PEEP group.
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Lucangelo, Umberto, and Massimo Ferluga. Pulmonary mechanical dysfunction in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0084.
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In intensive care units practitioners are confronted every day with mechanically-ventilated patients and should be able to sort out from all the data available from modern ventilators to tailored patient ventilatory strategy. Real-time visualization of pressure, flow and tidal volume provide valuable information on the respiratory system, to optimize ventilatory support and avoiding complications associated with mechanical ventilation. Early determination of patient–ventilator asynchrony, air-trapping, and variation in respiratory parameters is important during mechanical ventilation. A correct evaluation of data becomes mandatory to avoid a prolonged need for ventilatory support. During dynamic hyperinflation the lungs do not have time to reach the functional residual capacity at the end of expiration, increasing the work of breathing and promoting patient-ventilator asynchrony. Expiratory capnogram provides qualitative information on the waveform patterns associated with mechanical ventilation and quantitative estimation of expired CO2. The concept of dead space accounts for those lung areas that are ventilated but not perfused. Calculations derived from volumetric capnography are useful indicators of pulmonary embolism. Moreover, alveolar dead space is increased in acute lung injury and its value decreased in case of positive end-expiratory pressure (PEEP)-induced recruitment, whereas PEEP-induced overdistension tends to increment alveolar dead space.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Garner, Justin, and David Treacher. Intensive care unit and ventilation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0009.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by rapidly developing hypoxaemic respiratory failure and bilateral pulmonary infiltrates on chest X-ray. ALI/ARDS are a relatively frequent diagnosis in protracted-stay patients in the intensive care unit. The pathology is a non-specific response to a wide variety of insults. Impaired gas exchange, ventilation-perfusion mismatch, and reduced compliance ensue. Mechanical ventilation is the mainstay of management, along with treatment of the underlying cause. Mortality remains very high at around 40%. The condition is challenging to treat. Injury to the lungs, indistinguishable from that of ARDS, has been attributed to the use of excessive tidal volumes, pressures, and repeated opening and collapsing of alveoli. Lung-protective strategies aim to minimize the effects of ventilator-induced lung injury. Use of low tidal volume ventilation has been shown to improve mortality. Emerging ventilatory therapies include high-frequency oscillatory ventilation and extracorporeal membrane oxygenation.
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Lumb, Andrew B., and Natalie Drury. Respiratory physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0002.
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Moving away from the structure of traditional texts, this chapter follows the journey of oxygen molecules as they move from inspired air to their point of use in mitochondria, with some digressions along the way to cover other relevant aspects of respiratory physiology. The chapter encompasses all the key aspects of respiratory physiology and also highlights physiological alterations that occur under both general and regional anaesthesia, moving the physiological principles discussed into daily anaesthetic practice. The chapter explores relevant anatomy of the airways, lungs, and pleura. The histology and function of the airway lining and alveoli are described, so illustrating the importance of pulmonary defence mechanisms for protecting the internal milieu of the body from this large and fragile interface with the outside world. Key principles and concepts including resistance, compliance, and diffusion are all discussed in their clinical context. Concepts relating to the mechanics of breathing and the control of airway diameter are considered along with lung volumes and their measurement. Both the central and peripheral mechanisms involved in the control of breathing are discussed with particular attention to the impact of anaesthesia. The relationship between ventilation and perfusion and the carriage of oxygen and carbon dioxide are all discussed in detail. The principles behind key respiratory measurements such as dead space, lung volumes, diffusing capacity, and shunt are all described. Overall the chapter provides a comprehensive review of respiratory physiology as well as including additional aspects of variation that occur under anaesthesia.
Book chapters on the topic "Alveolar air"
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McGuire, Anna L., and R. Sudhir Sundaresan. "Management of Persistent Post-operative Alveolar Air Leak." In Difficult Decisions in Surgery: An Evidence-Based Approach, 207–28. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6404-3_17.
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Santos, Paulo, Valentina Vassilenko, Carolina Conduto, Jorge M. Fernandes, Pedro C. Moura, and Paulo Bonifácio. "Pilot Study for Validation and Differentiation of Alveolar and Esophageal Air." In IFIP Advances in Information and Communication Technology, 331–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78288-7_32.
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Kreyling, W. G., and M. Neuner. "Effect of Ambient Air on a Particle Clearance Parameter of Canine Alveolar Macrophages." In Environmental Hygiene II, 217–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-46712-7_50.
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Meissner, S., L. Knels, T. Koch, E. Koch, S. Adami, X. Y. Hu, and N. A. Adams. "Experimental and Numerical Investigation on the Flow-Induced Stresses on the Alveolar-Epithelial-Surfactant-Air Interface." In Notes on Numerical Fluid Mechanics and Multidisciplinary Design, 67–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-20326-8_4.
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Sembulingam, K., and Prema Sembulingam. "Inspired Air, Alveolar Air and Expired Air." In Essentials of Medical Physiology, 633. Jaypee Brothers Medical Publishers (P) Ltd., 2006. http://dx.doi.org/10.5005/jp/books/10283_123.
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Sembulingam, K., and Prema Sembulingam. "Inspired Air, Alveolar Air and Expired Air." In Essentials of Medical Physiology, 673. Jaypee Brothers Medical Publishers (P) Ltd., 2010. http://dx.doi.org/10.5005/jp/books/11093_123.
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Sembulingam, K., and Prema Sembulingam. "Inspired Air, Alveolar Air and Expired Air." In Essentials of Medical Physiology, 703. Jaypee Brothers Medical Publishers (P) Ltd., 2012. http://dx.doi.org/10.5005/jp/books/11696_36.
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Bourke, S. J., and G. P. Spickett. "Diffuse alveolar haemorrhage." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4235–38. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0421.
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Diffuse alveolar haemorrhage is characterized by acute respiratory failure, diffuse air space shadowing on the chest radiograph, haemoptysis, and anaemia. There are many different causes including immune-mediated diseases (notably pulmonary vasculitis, connective tissue diseases, and Goodpasture’s syndrome) and non-immune-mediated disease (cardiac failure, infection, coagulation disorders, thrombolytic therapy, toxins, and barotrauma). Prompt identification of the underlying cause is important in directing specific treatments. Goodpasture’s syndrome is an autoimmune disorder characterized by alveolar haemorrhage and glomerulonephritis due to antibasement membrane antibodies. Renal failure is usually the dominant feature, but alveolar haemorrhage can precede renal involvement. Idiopathic pulmonary haemosiderosis is a rare disorder of unknown cause with recurrent alveolar bleeding, which may provoke pulmonary fibrosis, and anaemia.
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Bourke, S. J. "Pulmonary alveolar microlithiasis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4265–67. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0430.
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Pulmonary alveolar microlithiasis is characterized by the deposition of calcium phosphate in the alveolar air spaces as a result of mutations of the SLC34A2 gene. The diagnosis is often made before symptoms have developed when a chest radiograph is performed for other reasons, and shows a dramatic typical ‘sandstorm’ pattern of diffuse bilateral calcified micronodules. The patient is often symptom-free when the diagnosis is made after a chest radiograph is taken incidentally and reveals calcified micronodules, but typically the disease progresses to respiratory failure over about 10–20 years. Etidronate has led to improvement in some cases that have been detected early. Lung transplantation is the main option in advanced disease. The severity of the disease and prognosis are variable, and this may be influenced by the specific type of gene mutation. Survival of 10–20 years from the onset of symptoms is typical.
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"Respiratory and cardiovascular system." In Oxford Assess and Progress: Medical Sciences, edited by Jade Chow, John Patterson, Kathy Boursicot, and David Sales. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199605071.003.0021.
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Oxidative metabolism is essential for our cellular life. Although tissues such as skeletal muscle can operate for short periods anaerobically, human life does not continue for long in the absence of a ready supply of oxygen. Adequate oxygen delivery to tissues is essential for aerobic metabolism and disorders of delivery ultimately become life-threatening. The factors contributing to oxygen delivery are summarised in the oxygen flux equation: OXYGEN FLUX = CARDIAC OUTPUT × ARTERIAL OXYGEN CONTENT The cardiac output is the product of heart rate and stroke volume and amounts to about 5 litres per minute. The arterial oxygen content is the product of the blood’s haemoglobin concentration multiplied by the haemoglobin’s % saturation. The latter is determined by the partial pressure of oxygen in the blood. This is higher in arterial than in venous blood. A small, additional amount of oxygen is carried dissolved in the blood, the amount again determined by the oxygen partial pressure. The five litres of arterial blood delivered to the tissues each minute contain about 1000ml of oxygen. Only a quarter of this (250ml) is needed to support resting metabolism. There is therefore a large safety factor in oxygen delivery. This can be utilized, in concert with adaptive changes to cardiac output, vascular resistance and pulmonary ventilation, in situations such as muscular exercise, where oxygen demand increases dramatically, or at high altitude where inspired oxygen is low. Oxygen delivery depends on the cardiovascular system, respiratory system and the blood. In the lungs, blood in the alveoli is brought into close proximity with alveolar air so that oxygen can diffuse easily into the blood and carbon dioxide, a major waste product of metabolism, can diffuse into the alveolar air. Alveolar air is kept refreshed with atmospheric air by pulmonary ventilation which keeps the partial pressures of oxygen and carbon dioxide in alveolar air and pulmonary capillary blood in a constant equilibrium. This process ensures that pulmonary venous blood and systemic arterial blood have high oxygen and low carbon dioxide partial pressures. Once in the blood, almost all of the oxygen combines with haemoglobin and is transported by the cardiovascular system to the tissues.
Conference papers on the topic "Alveolar air"
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Gaver, Donald P., Melissa A. Krueger, and Samir N. Ghadiali. "The Influence of Surfactant Physicochemical Properties on Pulmonary Interfacial Flow Analogues." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0218.
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Abstract Many of the lung’s mechanical properties are influenced by pulmonary surfactant physicochemical characteristics. Pulmonary surfactant is a complex lipid-protein mixture formed in the type II alveolar cells and secreted into the alveolar subphase [1]. These substances reduce the surface tension at the air-liquid interface of the lining fluid that coats the interior of the lung. At sufficiently high concentrations, pulmonary surfactant reduces the surface tension to near zero and. in the process, stabilizes the alveoli and small airways [2–4].
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Di Francesco, F., S. Tabucchi, C. Loccioni, M. Ferro, and G. Pioggia. "Development of a CO2 triggered alveolar air sampler." In 2007 IEEE International Symposium on Industrial Electronics. IEEE, 2007. http://dx.doi.org/10.1109/isie.2007.4375061.
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de Silva, Geethanga, and Fred R. Beyette. "Alveolar air Volatile Organic Compound extractor for clinical breath sampling." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944839.
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Vikranth, T., T. Dale, M. Haris, and N. Forsyth. "Decellularised porcine pleural patches for management of prolonged alveolar air leaks." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.41.
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Cutillo, Antonio G., David C. Ailion, Krishnamurthy Ganesan, Alan H. Morris, and Carl H. Durney. "Alveolar air-tissue interface and nuclear magnetic resonance behavior of the lung." In Medical Imaging 1995, edited by Eric A. Hoffman. SPIE, 1995. http://dx.doi.org/10.1117/12.209686.
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Son, Y., C. Carranza, M. Torres, K. Black, L. E. Jones, Q. Meng, A. R. Osornio-Vargas, and S. Schwander. "Association Between Particle Load in Alveolar Macrophages and Air Pollution Particulate Matter Exposures in México City." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3175.
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Winchester, L. W., and R. L. Leonard. "Optical properties of blue jay feathers." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.wo2.
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The source of the blue color of blue jay feathers has been attributed to scattering since the mid-nineteenth century after it was found that no pigments could be extracted from the feathers. The transmittance and scattering properties of blue jay feathers were measured as a function of wavelength between 0.36 and 0.74 μm. The transmittance in the red region of the spectrum was found to be considerably higher than the transmittance in the blue region. The peak transmittance occurs at a wavelength of 0.63 μm. Scattering measurements revealed an intensity maximum at shorter wavelengths and a minimum at longer wavelengths. A computer analysis of the scattered intensity yielded an exponential dependence on wavelength. The exponent ranged from −3.98 to −4.44 for diffuse scattering geometries and −2.67 for the specular scattering geometries compared with the value of −4.0 expected for Rayleigh scattering. The feathers used in this experiment were rectrices. The barbs have a transparent outer layer underlain by a layer of box cells or alveolar cells, beneath which there is a dark layer of melanin-containing cells. The alveolar cells contain irregularly shaped air cavities ranging in size from 0.03 to 0.3 μm. The air cavities are responsible for the scattering dependence.
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Shirai, A., and T. Hayase. "Effect of Retention Time of Neutrophils in Alveolar Capillaries on Increase in Their Concentration in the Capillary Network." In ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37653.
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It is said that neutrophils, a kind of leukocytes, can be retained in pulmonary alveolar capillary bed, even in normal lungs, resulting in higher concentration than in systemic circulation due to their relatively low deformability, and the concentrated neutrophils help the lung to effectively eliminate the enemies invading from outer air. The authors have developed a model to simulate the flow of neutrophils through an alveolar capillary network, considering the cells’ low deformability as the dominant factor for the retention. Flow of a suspension of neutrophils in plasma through a simplified lattice alveolar capillary network model was numerically simulated to investigate the effect of the retention on the increase in the concentration ratio of the cells between in the network and in the suspension. The numerical result showed that the ratio was lower than the experimentally obtained value. Other possible factors to influence the cell’s retention time are friction and adhesion of the cell on the endothelium. In the last study, effect of the retention time of the cells in individual capillary segments on the increase in the concentration ratio was investigated to suggest the ratio may have an upper limit no matter how long the retention time is extended. In this paper, the authors investigated the contribution of various parameters which affect transit time of a neutrophil through a single capillary segment to the relationships between the retention time and the concentration ratio. Finally, it was shown that the number of cells in the network increased to approach a finite value as the increase in the coefficient, independent of the cell property, concentration of the cells in the suspension or the capillary shape. Transition of the relationship was changed with the parameters.
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Abo, K., and A. Wilson. "Human induced pluripotent stem cell-derived alveolar type 2 cells mature at air-liquid interface and respond to airborne stimuli." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4648.
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Frank, Andreas O., and C. J. Charles Chuong. "Modelling of Oxygen Diffusion in Pulmonary Capillaries." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0220.
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Abstract Oxygen (O2) uptake by the lungs occurs from the alveolar air space to hemoglobin (Hb) in the red blood cell (RBC), which can conceptually be separated into membrane and red cell segments (Roughton and Forster Equation) [8]. The objective of this study was to determine O2 uptake using the finite element method (FEM) and assess the effects of geometry. We developed a modified 2D model representing the sheet flow characteristics of the pulmonary capillaries [2]. Analysis of an axisymmetric model of comparable hematocrit (Hct) was also carried out. The Nusselt number was used to assess the efficiency in oxygen transport of these two geometric configurations.
Reports on the topic "Alveolar air"
1
Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.
Full textAbstract:
Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmosphere for a long time with a small aerodynamic size (≤2.5μm) and large specific surface area which is attached to a variety of toxic and harmful substances . PM2.5 can deposite under the trachea of the respiratory tract, reaching deep into the alveolar area, damaging alveolar macrophages and type Ⅱ alveolar epithelial cells, inducing alveolar inflammation, resulting in decreased immunity of the respiratory tract and interfering with normal physiological functions of the lungs.
2
Villegas Aguilar, Julio Cesar, Marco Felipe Salas Orozco, Maria de los Angeles Moyaho Bernal, Eric Reyes Cervantes, Julia Flores-Tochihuitl, Alberto Vinicio Jerezano Domínguez, and Miguel Angel Casillas Santana. Mechanical vibrations and increased alveolar bone density in animal models as an alternative to improve bone quality during orthodontic treatment: A systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0103.
Full textAbstract:
Review question / Objective: The aim of this systematic review is to determine whether mechanical vibration increases alveolar bone density in animals models and their possible application during orthodontic treatment. In this sense, the focused question is: Is the increase in alveolar bone density by mechanical vibrations in animal models an alternative to improve bone quality during orthodontic treatment? Eligibility criteria: All published animal studies will be included. Animal studies where high or low frequency vibrations were be applied, Articles where density or osteogenesis were be measured and compared to a control group. All publications will be considered except for those where the full-text article will not available, or the authors’ affiliation or the place of publication will not be specified. Only articles published in English.