دورية أكاديمية
أعرض في EDS

Three Alveolar Phenotypes Govern Lung Function in Murine Ventilator-Induced Lung Injury.

التفاصيل البيبلوغرافية
العنوان: Three Alveolar Phenotypes Govern Lung Function in Murine Ventilator-Induced Lung Injury.
المؤلفون: Smith BJ; Department of Bioengineering, College of Engineering, Design & Computing, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, United States.; Department of Pediatric Pulmonary and Sleep Medicine, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States., Roy GS; Vermont Lung Center, Larner College of Medicine, The University of Vermont, Burlington, VT, United States., Cleveland A; Vermont Lung Center, Larner College of Medicine, The University of Vermont, Burlington, VT, United States., Mattson C; Department of Bioengineering, College of Engineering, Design & Computing, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, United States., Okamura K; Department of Bioengineering, College of Engineering, Design & Computing, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, United States., Charlebois CM; Vermont Lung Center, Larner College of Medicine, The University of Vermont, Burlington, VT, United States., Hamlington KL; Department of Pediatric Pulmonary and Sleep Medicine, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States., Novotny MV; Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States., Knudsen L; Institute of Functional and Applied Anatomy, Hannover Medical School, Hanover, Germany.; Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research, Hanover, Germany., Ochs M; Institute of Functional Anatomy, Charité Medical University of Berlin, Berlin, Germany., Hite RD; Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States.; Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, College of Medicine, University of Cincinnati, Cincinnati, OH, United States., Bates JHT; Vermont Lung Center, Larner College of Medicine, The University of Vermont, Burlington, VT, United States.
المصدر: Frontiers in physiology [Front Physiol] 2020 Jun 30; Vol. 11, pp. 660. Date of Electronic Publication: 2020 Jun 30 (Print Publication: 2020).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101549006 Publication Model: eCollection Cited Medium: Print ISSN: 1664-042X (Print) Linking ISSN: 1664042X NLM ISO Abbreviation: Front Physiol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Research Foundation
مستخلص: Mechanical ventilation is an essential lifesaving therapy in acute respiratory distress syndrome (ARDS) that may cause ventilator-induced lung injury (VILI) through a positive feedback between altered alveolar mechanics, edema, surfactant inactivation, and injury. Although the biophysical forces that cause VILI are well documented, a knowledge gap remains in the quantitative link between altered parenchymal structure (namely alveolar derecruitment and flooding), pulmonary function, and VILI. This information is essential to developing diagnostic criteria and ventilation strategies to reduce VILI and improve ARDS survival. To address this unmet need, we mechanically ventilated mice to cause VILI. Lung structure was measured at three air inflation pressures using design-based stereology, and the mechanical function of the pulmonary system was measured with the forced oscillation technique. Assessment of the pulmonary surfactant included total surfactant, distribution of phospholipid aggregates, and surface tension lowering activity. VILI-induced changes in the surfactant included reduced surface tension lowering activity in the typically functional fraction of large phospholipid aggregates and a significant increase in the pool of surface-inactive small phospholipid aggregates. The dominant alterations in lung structure at low airway pressures were alveolar collapse and flooding. At higher airway pressures, alveolar collapse was mitigated and the flooded alveoli remained filled with proteinaceous edema. The loss of ventilated alveoli resulted in decreased alveolar gas volume and gas-exchange surface area. These data characterize three alveolar phenotypes in murine VILI: flooded and non-recruitable alveoli, unstable alveoli that derecruit at airway pressures below 5 cmH 2 O, and alveoli with relatively normal structure and function. The fraction of alveoli with each phenotype is reflected in the proportional changes in pulmonary system elastance at positive end expiratory pressures of 0, 3, and 6 cmH 2 O.
(Copyright © 2020 Smith, Roy, Cleveland, Mattson, Okamura, Charlebois, Hamlington, Novotny, Knudsen, Ochs, Hite and Bates.)
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معلومات مُعتمدة: K99 HL128944 United States HL NHLBI NIH HHS; R01 HL124052 United States HL NHLBI NIH HHS; R00 HL128944 United States HL NHLBI NIH HHS; R01 HL142702 United States HL NHLBI NIH HHS; R01 GM123010 United States GM NIGMS NIH HHS; F31 HL149268 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: alveolar mechanics; lung function; pulmonary surfactant; stereology; ventilator-induced lung injury
تواريخ الأحداث: Date Created: 20200723 Latest Revision: 20240329
رمز التحديث: 20240329
مُعرف محوري في PubMed: PMC7338482
DOI: 10.3389/fphys.2020.00660
PMID: 32695013
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-042X
DOI:10.3389/fphys.2020.00660