Abstract
The human lung is exquisitely structured to carry out the essential function of gas exchange. The architecture of the lung is characterized by generations of dichotomous branching airways and vessels resulting in the generation of an enormous total surface area for gas exchange. The extremely thin alveolar-capillary membrane is optimized for the transfer of oxygen from the airspaces to the blood compartment and the removal of carbon dioxide from the blood compartment to the airspaces. Majority of the surface area of the alveolar membrane consists of alveolar epithelial type 1 cells; however, alveolar surface tension and fluid homeostasis is maintained mainly by alveolar epithelial type 2 cells. The lung is constantly exposed to environmental particulate matters, antigens, aspirated particles, and inhaled microbial pathogens, but is protected by a complex immune defense mechanism comprised of the mucociliary clearance system, secreted molecules, recruited neutrophils, the mononuclear phagocyte system, dendritic cells, T cells, and B cells. However, the delicate structure of the lungs, evolutionarily designed to optimally serve the core function of gas exchange, predisposes the lungs to injury, and as presented in the following chapters, abnormalities of the hematologic system can lead to acute lung dysfunction.
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Acknowledgements
The authors are supported by research funding from the National Heart, Lung and Blood Institute (Award Number: HL086884) and the National Institute for Allergy and Infectious Diseases (Award Number: AI119042).
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Zhang, P., Lee, J.S. (2017). The Lung–Blood Interface. In: Lee, J., Donahoe, M. (eds) Hematologic Abnormalities and Acute Lung Syndromes. Respiratory Medicine. Humana Press, Cham. https://doi.org/10.1007/978-3-319-41912-1_1
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DOI: https://doi.org/10.1007/978-3-319-41912-1_1
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