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Related Concept Videos

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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Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
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Related Experiment Video

Updated: May 14, 2026

Quantifying Pulmonary Microvascular Density in Mice Across Lobules
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Published on: January 3, 2025

Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction.

Eliana S Mendes1, Jose Eduardo D Cancado1, Patricia Rebolledo1

  • 1Division of Pulmonary, Critical Care and Sleep Medicine, University of Miami Miller School of Medicine, Miami, FL.

Chest
|January 26, 2013
PubMed
Summary

Healthy smokers show impaired airway vascular endothelial function, which improves with inhaled glucocorticosteroids (ICS). This suggests airway dysfunction may precede systemic issues in smokers.

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Published on: October 22, 2014

Area of Science:

  • Pulmonary Medicine
  • Vascular Biology
  • Respiratory Pharmacology

Background:

  • Cigarette smoking is linked to systemic endothelial dysfunction.
  • Airway circulation's direct exposure to smoke suggests potential localized vascular impairment.
  • This study investigates airway endothelial function in healthy smokers without systemic dysfunction.

Purpose of the Study:

  • To compare airway and systemic endothelial function in lung-healthy smokers.
  • To measure systemic inflammation markers in smokers.
  • To assess the effect of inhaled glucocorticosteroids (ICS) on airway endothelial function and inflammation.

Main Methods:

  • Compared 15 healthy smokers with 17 healthy non-smokers.
  • Assessed airway endothelial function via albuterol-induced blood flow (ΔQaw) and systemic function via brachial artery flow-mediated dilation (FMD).
  • Smokers received 3-week treatments of ICS or placebo in a crossover design; measured C-reactive protein and IL-6.

Main Results:

  • Smokers had significantly lower baseline airway blood flow (ΔQaw) than non-smokers (1% vs. 45%).
  • ICS treatment normalized airway blood flow in smokers (to 41%) but did not affect systemic FMD or inflammatory markers.
  • The response to ICS was related to baseline airway endothelial function.

Conclusions:

  • Healthy smokers exhibit impaired airway vascular endothelial function, potentially preceding systemic endothelial dysfunction.
  • Inhaled glucocorticosteroids (ICS) can restore airway endothelial function in smokers.
  • Airway endothelial function impairment may be an early marker of smoking-related vascular damage.