Experimental Lung Research Research Articles

Intranasal versus intratracheal exposure to lipopolysaccharides in a murine model of acute respiratory distress syndrome

Due to frequent and often severe lung affections caused by COVID-19, murine models of acute respiratory distress syndrome (ARDS) are increasingly used in experimental lung research. The one induced by a single lipopolysaccharide (LPS) exposure is practical. However, whether it is preferable to administer LPS intranasally or intratracheally remains an open question. Herein, female C57Bl/6 J mice were exposed intranasally or intratracheally to one dose of either saline or 3 mg/kg of LPS. They were studied 24 h later. The groups treated with LPS, either intranasally or intratracheally, exhibited a pronounced neutrophilic inflammation, signs of lung tissue damage and protein extravasation into the alveoli, and mild lung dysfunction. The magnitude of the response was generally not different between groups exposed intranasally versus intratracheally. However, the variability of some the responses was smaller in the LPS-treated groups exposed intranasally versus intratracheally. Notably, the saline-treated mice exposed intratracheally demonstrated a mild neutrophilic inflammation and alterations of the airway epithelium. We conclude that an intranasal exposure is as effective as an intratracheal exposure in a murine model of ARDS induced by LPS. Additionally, the groups exposed intranasally demonstrated less variability in the responses to LPS and less complications associated with the sham procedure.

Implementation of an experimental isolated lung perfusion model on surgically resected human lobes

Isolated lung perfusion (ILP) is an ideal model to study treatment effects on a variety of pathologies. As published research mostly relies on rejected donor lungs or animal organs, this study investigates the use of surgically resected human lobes as an alternative and novel model for personalized experimental research. Ten surgically resected lobes were perfused in acellular and normothermic condition. The indication for surgery was lung cancer. Perfusion and ventilation were adapted to the size of the lobes and both functional and metabolic parameters were assessed during ILP. Patients (age 67.5 y (59–81)|♀n = 3|♂n = 7) underwent anatomic pulmonary lobectomy. Ischemic time between arterial ligation and ILP was 226 minutes (161–525). Median duration of ILP was 135 (87–366) minutes. Gas exchange and mechanical respiratory parameters remained steady during ILP (pulmonary venous pO2 196(151–219) mmHg | peak AWP: 14.5(11–22) cmH2O). Metabolism stayed constant during ILP (Glucose consumption: 1.86 mg/min/LTLC (95%CI: −2.09 to −1.63) | lactate production: 0.005 mmol/min/ LTLC (95%CI: 0.004 to 0.007)). ILP of surgically resected human lobes is a feasible and promising method. By maintaining a near physiological setting, this model may pave the way for future experimental lung research including cancer research, transplantation, physiology, pharmacology and mechanical ventilation.

Characterization of surfactant alterations in pigs infected with Actinobacillus pleuropneumoniae

ABSTRACTPurpose/Aim of the study: Surfactant, a surface active complex of phospholipids and proteins located at the inner surface of alveoli and small conducting airways is necessary for breathing. Bacterial respiratory tract infections frequently lead to surfactant alterations and to an increase in surface tension. Pigs, often used in experimental lung research, could suffer from severe pleuropneumonia, a highly contagious disease often characterized by sudden onset, short clinical course, high morbidity, and high mortality. It is caused by the gram-negative bacterium Actinobacillus pleuropneumoniae (A.pp.). This study tests the hypothesis that also in the subacute stage pathomorphological lung alterations are accompanied with increased inactive surfactant components. Clinical lung scores, functional and ultrastructural analysis of porcine surfactant were performed in pigs before infection and in the subacute state of infection. Clinical signs were determined using inter alia different subscores. Surfactant was isolated from the BALF for functional and quantitative ultrastructural studies. Results: In the subacute stage clinical, ultrosonographic and radiographic scores as well as the overall Respiratory Health Score showed significantly higher values than before infection. However, surfactant surprisingly contained more active surfactant subtypes and significantly less inactive subtypes such as unilamellar vesicles. The quantity of multilamellar vesicles with unclear function did not differ. The minimal surface tension of surfactant before and after infection was comparable. Conclusions: Thus, in spite of continued severe lung tissue alterations the surfactant system show signs of recovery. This may be the result of an effective adaption to inflammatory lung disorders caused by swine-specific pathogens.

Miniaturized bronchoscopy enables unilateral investigation, application, and sampling in mice.

Lung diseases, including pneumonia and asthma, are among the most prevalent human disorders, and murine models have been established to investigate their pathobiology and develop novel treatment approaches. Whereas bronchoscopy is valuable for diagnostic and therapeutic procedures in patients, no equivalent for small rodents has been established. Here, we introduce a miniaturized video-bronchoscopy system offering new opportunities in experimental lung research. With an outer diameter of 0.75 mm, it is possible to advance the optics into the main bronchi of mice. An irrigation channel allows bronchoalveolar lavage and unilateral application of substances to one lung. Even a unilateral infection is possible, enabling researchers to use the contralateral lung as internal control.

In vivo assessments of mucus dynamics in the rat lung using a Gd‐Cy5.5‐bilabeled contrast agent for magnetic resonance and optical imaging

Dysfunctions in mucociliary clearance are associated with the accelerated loss of lung function in several respiratory diseases. Approaches enabling the in vivo visualization of mucus dynamics in rodents at high resolution and sensitivity would be beneficial for experimental lung research. We describe the synthesis and characterization of two bilabeled amino dextran-based probes binding specifically to mucin. Labeling of secreted mucus and of mucin in goblet cells in the lungs of lipopolysaccharide-challenged rats has been demonstrated in vivo with near-infrared fluorescence and MRI and confirmed by histology. The effects of uridine triphosphate were then studied in lipopolysaccharide-challenged rats by simultaneously administering the imaging probe and the compound. The data suggest that uridine triphosphate increased the mucociliary clearance, but at the same time induced a release of mucin from goblet cells, thus not contributing to the overall reduction of mucus in the lung. The approach outlined here enables one to derive information on mucus clearance, as well as secretion. Such a global view on mucus dynamics may prove invaluable when testing new pharmacological agents aimed at improving mucociliary clearance.

Pathways of Proliferation

See related article, pages 1155–1163 Excessive proliferation of vascular smooth muscle cells (VSMCs) contributes to the pathogenesis of many cardiovascular diseases, including atherosclerosis and pulmonary arterial hypertension (PAH). VSMC proliferation also underlies the failure of many therapies, notable examples being restenosis following coronary angioplasty, vein graft failure in patients with coronary artery bypass grafts, and transplant vasculopathy. Few therapies directly target excess VSMC proliferation, in part, because the underlying pathways have been unknown. Recently, several pathways of VSMC proliferation have been defined, and new therapeutic targets have emerged. An example of the power of preventing VSMC proliferation in reducing human cardiovascular disease is the rapamycin (sirolimus)-coated coronary stent. After dozens of agents failed to prevent the 30% restenosis rate postangioplasty, this VSMC proliferation inhibitor reduced the number to ≈6%.1 However, rapamycin has toxicities, limiting its systemic use. Moreover, the mechanisms of accelerated VSMC proliferation may vary by disease, and, thus, the efficacy of an antiproliferative drug will likely be contextual (ie, disease dependent). Understanding the pathways controlling proliferation offers hope for identifying drugs that selectively target proliferating cells. The contribution by Gizard et al in this issue of Circulation Research identifies such a pathway and suggests new therapeutic targets.2 Members of this group expand on their previous work showing that peroxisome proliferator-activated receptor (PPAR)α activation suppresses G1→S cell cycle progression by increasing the expression of the cyclin dependent kinase (CDK) inhibitor p16INK4a.3 The present study is built on a solid body of knowledge of the cell cycle. Although growth factors are necessary to initiate proliferation in normal cells, cells become independent of these external stimuli during the G1 phase. This “point of no return” is highly regulated by the interaction among cyclins, CDKs, and CDK inhibitors.4 In nonproliferating cells, the …

Animal models of pulmonary fibrosis: how far from effective reality?

idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease, associated with high mortality rates and unresponsive to currently available treatments. Animal models are critical to identify and validate new therapeutic drug targets, a concept that is nicely highlighted by the review

Lung MRI for experimental drug research

Current techniques to evaluate the efficacy of potential treatments for airways diseases in preclinical models are generally invasive and terminal. In the past few years, the flexibility of magnetic resonance imaging (MRI) to obtain anatomical and functional information of the lung has been explored with the scope of developing a non-invasive approach for the routine testing of drugs in models of airways diseases in small rodents. With MRI, the disease progression can be followed in the same animal. Thus, a significant reduction in the number of animals used for experimentation is achieved, as well as minimal interference with their well-being and physiological status. In addition, under certain circumstances the duration of the observation period after disease onset can be shortened since the technique is able to detect changes before these are reflected in parameters of inflammation determined using invasive procedures. The objective of this article is to briefly address MRI techniques that are being used in experimental lung research, with special emphasis on applications. Following an introduction on proton techniques and MRI of hyperpolarized gases, the attention is shifted to the MRI analysis of several aspects of lung disease models, including inflammation, ventilation, emphysema, fibrosis and sensory nerve activation. The next subject concerns the use of MRI in pharmacological studies within the context of experimental lung research. A final discussion points towards advantages and limitations of MRI in this area.

Proton MRI as a noninvasive tool to assess elastase‐induced lung damage in spontaneously breathing rats

Elastase-induced changes in lung morphology and function were detected in spontaneously breathing rats using conventional proton MRI at 4.7 T. A single dose of porcine pancreatic elastase (75 U/100 g body weight) or vehicle (saline) was administered intratracheally (i.t.) to male Brown Norway (BN) rats. MRI fluid signals were detected in the lungs 24 hr after administration of elastase and resolved within 2 weeks. These results correlated with perivascular edema and cellular infiltration observed histologically. Reductions in MRI signal intensity of the lung parenchyma, and increases in lung volume were detected as early as 2 weeks following elastase administration and remained uniform throughout the study, which lasted 8 weeks. Observations were consistent with air trapping resulting from emphysema detected histologically. In a separate experiment, animals were treated daily intraperitoneally (i.p.) with all-trans-retinoic acid (ATRA; 500 microg/kg body weight) or its vehicle (triglyceride oil) starting on day 21 after elastase administration and continuing for 12 days. Under these conditions, ATRA did not elicit a reversal of elastase-induced lung damage as measured by MRI and histology. The present approach complements other validated applications of proton MRI in experimental lung research as a method for assessing drugs in rat models of respiratory diseases.

Do Urban Environmental Pollutants Exacerbate Childhood Lung Diseases?

Do Urban Environmental Pollutants Exacerbate Childhood Lung Diseases?

A new simple method of staining exogenous surfactant in experimental research.

Two commonly used techniques in experimental lung research have helped to determine which variables influence surfactant distribution within the lung: radioactive labelling of surfactant components and admixture of coloured microspheres to surfactant. However, neither technique allows the description of surfactant distribution at the alveolar level. The aim of this study was to establish a new technique using histology colourants for admixture to exogenous surfactant to make exogenous surfactant visible by light microscopy. In a step by step approach the authors evaluated the properties of a variety of green colourants when added to a natural porcine surfactant preparation for their ability to homogeneously mix with surfactant, to bind to surfactant, to adhere to a glass slide, to not be "overstained" by standard haematoxylin-eosin and Elastica van Giesson staining, to not influence in vitro surface tension properties of surfactant using a Wilhelmy balance, to not influence oxygenation and ventilation in a lung-lavage rat model and to preserve their colour and adherence to exogenous surfactant on lung specimens visualized by light microscopy. Only one of the tested green histology colourants (Green Dye) fulfilled all requirements and showed a brilliant green colour in a distribution pattern typical of surfactant at the alveolar level. It is concluded that the authors have established a new, simple and inexpensive method of staining exogenous surfactant for evaluation of its distribution by light microscopy at the alveolar level.

Chronic inhalation and biopersistence of refractory ceramic fiber in rats and hamsters.

Lifetime "nose-only" inhalation studies were conducted in rats using four types of refractory ceramic fibers (FCF), 1 micron in diameter x 22 to 26 microns length: High Purity, Kaolin, Zirconia, and After-Service; and on hamsters using Kaolin RCF. For comparison, animals also were exposed to chrysotile fibers. Rats were exposed 6 hr/day, 5 days/week for 24 months to concentrations ranging between 3 and 30 mg/m3. Time- and dose-dependent lesions in the rat included the development of interstitial fibrosis, pleural fibrosis, pulmonary tumors, and mesothelioma. Exposure to 3, 9 or 16 mg/m3 produced no excess lung tumors; no fibrosis was seen at 3 mg/m3. A significant increase in lung tumors and interstitial fibrosis was observed at 30 mg/m3. A single mesothelioma was observed in rats exposed to 9 mg/m3, while two occurred at 30 mg/m3. Hamsters were similarly exposed to 30 mg/m3 Kaolin RCF for 18 months; no lung tumors were induced, but pulmonary and pleural fibrosis were observed and there was a 42% incidence of mesothelioma. Multiple interim sacrifices together with recovery animals allowed detailed assessment of the lung burden of RCF, which was found to be dose related and, at the high doses, exceeded 10(5) fibers/mg of dry lung. During the various recovery periods there was a clear reduction in fiber burden. Mathematical modeling of these data for deposition, clearance, and retention and for species is currently underway.

Biochemistry and Pharmacology of Mucin-like Glycoproteins Produced by Cultured Airway Epithelial Cells

(1991). Biochemistry and Pharmacology of Mucin-like Glycoproteins Produced by Cultured Airway Epithelial Cells. Experimental Lung Research: Vol. 17, No. 3, pp. 533-545.

Lung Clearance of Inhaled Insoluble and Soluble Particles

Lung Clearance of Inhaled Insoluble and Soluble Particles

Issues in Biochemical Applications to Risk Assessment: How Do We Evaluate Individual Components of Multistage Models?

Research ArticleOpen AccessIssues in biochemical applications to risk assessment: how do we evaluate individual components of multistage models? M W Anderson M W Anderson National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Search for more papers by this author Published:1 December 1987https://doi.org/10.1289/ehp.8776175Cited by:4AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetailsCited by Portier C and Sherman C (1994) Potential Effects of Chemical Mixtures on the Carcinogenic Process within the Context of the Mathematical Multistage Model Toxicology of Chemical Mixtures, 10.1016/B978-0-12-768350-8.50031-1, (665-686), . Rogan W, Blanton P, Portier C and Stallard E (1991) Should the presence of carcinogens in breast milk discourage breast feeding?, Regulatory Toxicology and Pharmacology, 10.1016/0273-2300(91)90065-4, 13:3, (228-240), Online publication date: 1-Jun-1991. Kopp-Schneider A, Portier C and Rippmann F (1991) The application of a multistage model that incorporates DNA damage and repair to the analysis of initiation/promotion experiments, Mathematical Biosciences, 10.1016/0025-5564(91)90079-X, 105:2, (139-166), Online publication date: 1-Jul-1991. Sanders C, Lauhala K and McDonald K (2009) Tritiated Thymidine-Labeled Bronchioloalveolar Cells and Radiation Dose Following Inhalation of Plutonium in Rats, Experimental Lung Research, 10.3109/01902148909062859, 15:5, (755-769), Online publication date: 1-Jan-1989. Vol. 76December 1987Metrics About Article Metrics Publication History Originally published1 December 1987Published in print1 December 1987 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Macrophages, dust, and pulmonary diseases.

(1987). Macrophages, Dust, and Pulmonary Diseases. Experimental Lung Research: Vol. 12, No. 2, pp. 89-107.

Mucin biosynthesis and secretion in the respiratory tract.

Research ArticleOpen AccessMucin biosynthesis and secretion in the respiratory tract.is corrected byErrata: Mucin biosynthesis and secretion in the respiratory tract S S Spicer, and J R Martinez S S Spicer Search for more papers by this author and J R Martinez Search for more papers by this author Published:1 April 1984https://doi.org/10.1289/ehp.8455193Cited by:10AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetailsCited by Greeley M (2017) Immunopathology of the Respiratory System Immunopathology in Toxicology and Drug Development, 10.1007/978-3-319-47385-7_8, (419-453), . Kunkel S, Azimi P, Zhao H, Stark B and Stephens B (2017) Quantifying the size-resolved dynamics of indoor bioaerosol transport and control, Indoor Air, 10.1111/ina.12374, 27:5, (977-987), Online publication date: 1-Sep-2017. Wawegama N, Kanci A, Marenda M, Mansell P, Browning G and Markham P (2012) Histochemical and morphometric characterization of broncho-pneumonia in calves caused by infection with Mycoplasma bovis, Veterinary Microbiology, 10.1016/j.vetmic.2012.02.011, 158:1-2, (220-224), Online publication date: 1-Jul-2012. Redrow J, Mao S, Celik I, Posada J and Feng Z (2011) Modeling the evaporation and dispersion of airborne sputum droplets expelled from a human cough, Building and Environment, 10.1016/j.buildenv.2011.04.011, 46:10, (2042-2051), Online publication date: 1-Oct-2011. Even-Tzur N, Kloog Y, Wolf M and Elad D (2008) Mucus Secretion and Cytoskeletal Modifications in Cultured Nasal Epithelial Cells Exposed to Wall Shear Stresses, Biophysical Journal, 10.1529/biophysj.107.127142, 95:6, (2998-3008), Online publication date: 1-Sep-2008. NOBUYOSHI OTORI, BENGT CARLSÖÖ, PON (2009) Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development, Acta Oto-Laryngologica, 10.1080/00016489850154982, 118:2, (248-256), Online publication date: 1-Jan-1998. Samet J and Cheng P (2018) The role of airway mucus in pulmonary toxicology., Environmental Health Perspectives, 102:suppl 2, (89-103), Online publication date: 1-Jun-1994. Forstner J, Roomi N, Khorasani R, Kuhns W and Forstner G (1991) Effect of reserpine on the histochemical and biochemical properties of rat intestinal mucin, Experimental and Molecular Pathology, 10.1016/0014-4800(91)90026-T, 54:2, (129-143), Online publication date: 1-Apr-1991. Kim K (2009) Biochemistry and Pharmacology of Mucin-like Glycoproteins Produced by Cultured Airway Epithelial Cells, Experimental Lung Research, 10.3109/01902149109062863, 17:3, (533-545), Online publication date: 1-Jan-1991. Kim K, Nassiri J and Brody J (1989) Mechanisms of Airway Goblet Cell Mucin Release: Studies with Cultured Tracheal Surface Epithelial Cells, American Journal of Respiratory Cell and Molecular Biology, 10.1165/ajrcmb/1.2.137, 1:2, (137-143), Online publication date: 1-Aug-1989. Related articlesErrata: Mucin biosynthesis and secretion in the respiratory tract1 June 1984Environmental Health Perspectives Vol. 55April 1984Metrics About Article Metrics Publication History Originally published1 April 1984Published in print1 April 1984 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Mucin Biosynthesis and Secretion in the Respiratory Tract

Research ArticleOpen AccessMucin biosynthesis and secretion in the respiratory tract.is corrected byErrata: Mucin biosynthesis and secretion in the respiratory tract S S Spicer and J R Martinez S S Spicer Search for more papers by this author and J R Martinez Search for more papers by this author Published:1 April 1984https://doi.org/10.1289/ehp.8455193Cited by:10AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetailsCited by Greeley M (2017) Immunopathology of the Respiratory System Immunopathology in Toxicology and Drug Development, 10.1007/978-3-319-47385-7_8, (419-453), . Kunkel S, Azimi P, Zhao H, Stark B and Stephens B (2017) Quantifying the size-resolved dynamics of indoor bioaerosol transport and control, Indoor Air, 10.1111/ina.12374, 27:5, (977-987), Online publication date: 1-Sep-2017. Wawegama N, Kanci A, Marenda M, Mansell P, Browning G and Markham P (2012) Histochemical and morphometric characterization of broncho-pneumonia in calves caused by infection with Mycoplasma bovis, Veterinary Microbiology, 10.1016/j.vetmic.2012.02.011, 158:1-2, (220-224), Online publication date: 1-Jul-2012. Redrow J, Mao S, Celik I, Posada J and Feng Z (2011) Modeling the evaporation and dispersion of airborne sputum droplets expelled from a human cough, Building and Environment, 10.1016/j.buildenv.2011.04.011, 46:10, (2042-2051), Online publication date: 1-Oct-2011. Even-Tzur N, Kloog Y, Wolf M and Elad D (2008) Mucus Secretion and Cytoskeletal Modifications in Cultured Nasal Epithelial Cells Exposed to Wall Shear Stresses, Biophysical Journal, 10.1529/biophysj.107.127142, 95:6, (2998-3008), Online publication date: 1-Sep-2008. NOBUYOSHI OTORI, BENGT CARLSÖÖ, PON (2009) Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development, Acta Oto-Laryngologica, 10.1080/00016489850154982, 118:2, (248-256), Online publication date: 1-Jan-1998. Samet J and Cheng P (2018) The role of airway mucus in pulmonary toxicology., Environmental Health Perspectives, 102:suppl 2, (89-103), Online publication date: 1-Jun-1994. Forstner J, Roomi N, Khorasani R, Kuhns W and Forstner G (1991) Effect of reserpine on the histochemical and biochemical properties of rat intestinal mucin, Experimental and Molecular Pathology, 10.1016/0014-4800(91)90026-T, 54:2, (129-143), Online publication date: 1-Apr-1991. Kim K (2009) Biochemistry and Pharmacology of Mucin-like Glycoproteins Produced by Cultured Airway Epithelial Cells, Experimental Lung Research, 10.3109/01902149109062863, 17:3, (533-545), Online publication date: 1-Jan-1991. Kim K, Nassiri J and Brody J (1989) Mechanisms of Airway Goblet Cell Mucin Release: Studies with Cultured Tracheal Surface Epithelial Cells, American Journal of Respiratory Cell and Molecular Biology, 10.1165/ajrcmb/1.2.137, 1:2, (137-143), Online publication date: 1-Aug-1989. Related articlesErrata: Mucin biosynthesis and secretion in the respiratory tract1 June 1984Environmental Health Perspectives Vol. 55April 1984Metrics About Article Metrics Publication History Originally published1 April 1984Published in print1 April 1984 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Effect of hypoxia on incorporation of glucose carbons into lipids by isolated rat lung.

ARTICLESEffect of hypoxia on incorporation of glucose carbons into lipids by isolated rat lungDJ Bassett, AB Fisher, and JL RabinowitzDJ Bassett, AB Fisher, and JL RabinowitzPublished Online:01 Nov 1974https://doi.org/10.1152/ajplegacy.1974.227.5.1103MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByLung Lipid Composition and Surfactant BiologyMetabolic precursors of surfactant disaturated-phosphatidylcholine in preterms with respiratory distressJournal of Lipid Research, Vol. 50, No. 11Glucose homeostasis across human airway epithelial cell monolayers: role of diffusion, transport and metabolism10 September 2008 | Pflügers Archiv - European Journal of Physiology, Vol. 457, No. 5The Lung, Whole-Body Metabolism and Disease30 May 2008Effect of inflation on adenosine triphosphate catabolism and lactate production during normothermic lung ischemiaThe Annals of Thoracic Surgery, Vol. 55, No. 5A study on optimal temperature for isolated lung preservationThe Annals of Thoracic Surgery, Vol. 53, No. 1Allosteric control of 6-phosphofructo-1-kinase from rat lungComparative Biochemistry and Physiology Part B: Comparative Biochemistry, Vol. 101, No. 1-2Glutathione redox status of control and cadmium oxide‐exposed rat lungs during oxidant stressJournal of Toxicology and Environmental Health, Vol. 22, No. 3Lactate metabolism in fetal type II pneumocytesLung, Vol. 164, No. 1Oxygen Utilization and Toxicity in the Lungs1 January 2011Glucose and Intermediary Metabolism of the Lungs1 January 2011Isolated perfused lung preparation for studying altered gaseous environments.Environmental Health Perspectives, Vol. 56Pentose pathway of glucose metabolism in isolated granular pneumocytesBiochemical Pharmacology, Vol. 33, No. 8Intermediary metabolism of the lung.Environmental Health Perspectives, Vol. 55Effect of ischemia on fatty acid metabolism in fetal lungLife Sciences, Vol. 33, No. 6De novo fatty acid synthesis in developing rat lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 711, No. 1Glycerol kinase activity and glycerol metabolism of rat granular pneumocytes in primary cultureBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 711, No. 1Tissue Slices in the Study of Lung MetabolismThe Chemical Composition of the LungLung as a model for evaluation of critical intracellular PO2 and PCOA. B. Fisher, and C. Dodia1 July 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 241, No. 1Glucose metabolism accelerates the decline of hypoxic vasoconstriction in rat lungsRespiration Physiology, Vol. 44, No. 2Reutilization of fatty acid carbons for lung lipid synthesisJ. L. Rabinowitz, T. Cardwell, and D. J. Bassett1 April 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 240, No. 4Inhibitors of oxidative ATP production cause transient vasoconstriction and block subsequent pressor responses in rat lungs.Circulation Research, Vol. 48, No. 3Pathways of Palmitate Metabolism in the Isolated Rat Lung2 July 2009 | Experimental Lung Research, Vol. 2, No. 1Phospholipids of the lung in normal, toxic, and diseased states26 September 2008 | CRC Critical Reviews in Toxicology, Vol. 9, No. 3Fatty acid synthesis in the perfused rat lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 619, No. 2Pyridine nucleotides in lung and liver of hypoxic ratsLife Sciences, Vol. 26, No. 23Effect of perfusate glucose concentration on rat lung glycolysis.J S Kerr, N J Baker, D J Bassett, and A B Fisher1 March 1979 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 236, No. 3Pulmonary lipid biosynthesis: Simultaneous double-label in lipids from plasma, lung tissue and surfactant using a dog heart-lung preparationInternational Journal of Biochemistry, Vol. 8, No. 7Primary Pulmonary Responses to Toxic Agents26 September 2008 | CRC Critical Reviews in Toxicology, Vol. 5, No. 1 More from this issue > Volume 227Issue 5November 1974Pages 1103-1108 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.5.1103PubMed4440751History Published online 1 November 1974 Published in print 1 November 1974 Metrics

Effect of respiratory airflow rate on removal of soluble vapors by the nose.

Effect of respiratory airflow rate on removal of soluble vapors by the nose.