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Related Concept Videos

Physiological Control of Respiration01:23

Physiological Control of Respiration

Introduction
Breathing, a seemingly passive process, is regulated by the respiratory center in the brainstem. This center coordinates the involuntary control of respirations, which means it occurs without conscious effort, ensuring a smooth and uninterrupted pattern.
Regulation of Ventilation
The body maintains ventilation by monitoring levels of carbon dioxide (CO2), oxygen (O2), and hydrogen ion concentration (pH) in the arterial blood. Among these factors, the level of CO2 plays a crucial...
Pneumothorax II: Pathophysiology01:08

Pneumothorax II: Pathophysiology

Pneumothorax means the presence of air in the pleural space — the thin potential gap between the visceral and parietal pleura. This condition disrupts the normal pressure balance that keeps the lungs inflated, leading to partial or complete collapse of the affected lung.Normal physiologyUnder normal conditions, the pleural space maintains a slightly negative intrapleural pressure, which keeps the lungs expanded against the chest wall. This negative pressure creates a delicate balance between...
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
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:
Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure01:16

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure

Oxygen therapy has emerged as a significant tool in enhancing the quality of life for patients suffering from pulmonary arterial hypertension (PAH). While this therapy has principally been studied on patients with significant hypoxemia, this therapeutic approach helps prevent potential organ damage and can be administered in the comfort of one's home.
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue, improving...
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...

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Updated: Jun 22, 2026

Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
13:32

Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices

Published on: January 14, 2014

Hypoxic pulmonary vasoconstriction--invited article.

A Mark Evans1, Jeremy P T Ward

  • 1Centre for Integrative Physiology, College of Medicine and Veterinary Medicine, Hugh Robson Building University of Edinburgh, Edinburgh EH8 9XD, USA. Mark.Evans@ed.ac.uk

Advances in Experimental Medicine and Biology
|June 19, 2009
PubMed
Summary
This summary is machine-generated.

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive lung response to low oxygen. This review explores the controversial signaling pathways, including AMPK and redox signaling, that link mitochondrial oxygen sensing to vasoconstriction.

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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
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Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
13:32

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Published on: January 14, 2014

Oxygenation-sensitive Cardiac MRI with Vasoactive Breathing Maneuvers for the Non-invasive Assessment of Coronary Microvascular Dysfunction
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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
08:02

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Published on: October 19, 2013

Area of Science:

  • Physiology
  • Cellular Biology
  • Pulmonary Medicine

Background:

  • Hypoxic pulmonary vasoconstriction (HPV) is a vital adaptive mechanism redirecting blood flow from poorly ventilated lung areas to optimize gas exchange.
  • The precise molecular mechanisms underlying HPV, particularly the oxygen-sensing pathways within pulmonary arteries, remain incompletely understood.
  • Mitochondria are increasingly recognized as key oxygen sensors, with calcium (Ca2+) signaling and Rho kinase playing critical roles in sustained vasoconstriction.

Purpose of the Study:

  • To review the current understanding of hypoxic pulmonary vasoconstriction (HPV) mechanisms.
  • To discuss the evidence supporting different hypotheses for the signaling pathways linking oxygen sensing to HPV.
  • To clarify the role of mitochondria, calcium signaling, and redox pathways in HPV.

Main Methods:

  • Literature review of studies investigating HPV mechanisms.
  • Analysis of evidence supporting proposed signaling pathways: AMPK, Redox, and ROS hypotheses.
  • Discussion of experimental findings related to mitochondrial function, calcium dynamics, and ion channel activity in HPV.

Main Results:

  • Mitochondria are implicated as the primary oxygen sensors in pulmonary arteries.
  • Calcium (Ca2+) release from ryanodine-sensitive stores and Rho kinase activation are crucial for HPV.
  • Three main hypotheses (AMPK, Redox, ROS) exist regarding the signaling pathways, with ongoing debate about their validity and interplay.

Conclusions:

  • HPV is a complex process involving mitochondrial oxygen sensing and downstream signaling cascades.
  • The precise nature of the signaling pathways (AMPK vs. redox vs. ROS) linking oxygen sensing to vasoconstriction requires further elucidation.
  • Understanding these mechanisms is critical for addressing pulmonary vascular diseases.