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Related Concept Videos

Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation

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Related Experiment Video

Updated: Jun 5, 2026

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
10:37

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

Structure-function relations in an elastase-induced mouse model of emphysema.

Hiroshi Hamakawa1, Erzsébet Bartolák-Suki, Harikrishnan Parameswaran

  • 1Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA.

American Journal of Respiratory Cell and Molecular Biology
|December 21, 2010
PubMed
Summary
This summary is machine-generated.

Emphysema progression involves increasing airspace heterogeneity and lung function decline. Mechanical forces and remodeled collagen contribute to alveolar wall rupture, driving disease progression in mice.

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Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice
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Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice

Published on: September 26, 2019

Related Experiment Videos

Last Updated: Jun 5, 2026

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
10:37

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice
05:48

Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice

Published on: September 26, 2019

Area of Science:

  • Pulmonary Medicine
  • Biomedical Engineering
  • Pathology

Background:

  • Emphysema involves airspace destruction and lung function decline.
  • The relationship between structural changes and functional decline in emphysema is not fully understood.

Purpose of the Study:

  • To investigate the temporal changes in lung structure, mechanics, and extracellular matrix remodeling following elastolytic injury in a mouse model.
  • To establish structure-function relationships during emphysema progression.

Main Methods:

  • Mice were treated with porcine pancreatic elastase to induce emphysema.
  • Respiratory impedance, extracellular matrix composition, and lung histology were assessed at 2, 7, and 21 days post-treatment.
  • Network modeling was used to simulate parenchymal mechanics and alveolar wall rupture.

Main Results:

  • Emphysema induction led to increased respiratory compliance and variability by Day 21.
  • Airspace heterogeneity progressively increased over time.
  • Strong correlations were found between lung compliance and airspace size/heterogeneity, supporting a mechanical basis for disease progression.

Conclusions:

  • Progressive lung function decline in emphysema is linked to airspace heterogeneity.
  • Mechanical forces and collagen remodeling play a critical role in alveolar wall rupture and disease progression.