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Chronic Obstructive Pulmonary Disease II: Emphysema

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-II: Pathophysiology

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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:
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Chronic Obstructive Pulmonary Disease I: Introduction

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

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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...

Atelectasis II: Pathophysiology

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...

Pulmonary Edema II: Pathophysiology

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Related Experiment Video

Updated: May 19, 2026

Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice

Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice

Published on: September 26, 2019

Acute mechanical forces cause deterioration in lung structure and function in elastase-induced emphysema.

M V Szabari¹, H Parameswaran, S Sato

¹Dept. of Biomedical Engineering, Boston Univ., Boston, MA 02215, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology

|August 7, 2012

Summary

Deep inspirations in mice with emphysema induced acute lung structure and function changes, creating a potential model for acute exacerbations of chronic obstructive pulmonary disease (AECOPD). This study offers a new avenue for AECOPD research.

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Last Updated: May 19, 2026

Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice

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

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Published on: August 28, 2011

Area of Science:

Pulmonary Medicine
Biomedical Engineering
Animal Models

Background:

The relationship between chronic obstructive pulmonary disease (COPD) progression and exacerbations remains poorly understood.
A critical gap exists in the lack of a reliable animal model for acute exacerbations of COPD (AECOPD).

Purpose of the Study:

To investigate the impact of mechanical forces from deep inspirations (DIs) on short-term lung deterioration.
To establish a potential animal model that mimics AECOPD.

Main Methods:

Elastase-treated mice were subjected to ventilation with or without DIs at varying time points post-treatment.
Lung function was assessed using body plethysmography and forced oscillations.
Histological analysis quantified airspace diameters, alveolar wall thickness, septal ruptures, and airway attachment density.

Main Results:

Deep inspirations significantly altered lung function parameters (FRC, compliance, resistance, hysteresivity) in emphysematous mice.
At 21 days post-elastase treatment, DIs induced structural changes including increased alveolar wall thickness and septal ruptures, and decreased airway attachment density.
These functional and structural changes mimicked key aspects of AECOPD.

Conclusions:

Acute mechanical forces, such as DIs, can induce irreversible lung damage and functional impairment in emphysematous lungs once critical remodeling has occurred.
The application of DIs in mice with established emphysema presents a promising and viable model for studying AECOPD.