Related Experiment Video

Updated: Jul 10, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Iron homeostasis in the lung following asbestos exposure

Andrew J Ghio, Jacqueline Stonehuerner, Judy Richards

    Antioxidants & Redox Signaling
    |November 15, 2007
    PubMed

    More Related Videos

    Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition06:12

    Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

    Published on: March 3, 2023

    An Air-liquid Interface Bronchial Epithelial Model for Realistic, Repeated Inhalation Exposure to Airborne Particles for Toxicity Testing09:29

    An Air-liquid Interface Bronchial Epithelial Model for Realistic, Repeated Inhalation Exposure to Airborne Particles for Toxicity Testing

    Published on: May 13, 2020

    Related Concept Videos

    Atelectasis II: Pathophysiology01:10

    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...
    Acute Respiratory Failure-II01:21

    Acute Respiratory Failure-II

    Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
    The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
    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
    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...
    Pulmonary Cycle: Exhalation01:17

    Pulmonary Cycle: Exhalation

    In terms of human respiration, the act of expelling air, known as exhalation (or expiration), operates on the principle of pressure gradients. During expiration, the pressure within the lungs exceeds that of the surrounding atmosphere. Under normal conditions, quiet breathing involves passive exhalation and is free of muscular contractions. This is because the exhalation process is driven by the natural elastic recoil of the lungs and chest wall, both of which have an inherent tendency to...