Related Experiment Video

Updated: Aug 15, 2026

A Porcine Model of Acute Autologous Pulmonary Embolism
07:44

A Porcine Model of Acute Autologous Pulmonary Embolism

Published on: September 6, 2024

[The change of pulmonary surfactant associated protein A in acute pulmonary embolism]

Chun-ping Liu1, Yun-jian Zhang, Wei-xuan Lu

  • 1Department of Respiratory Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.

Zhonghua Jie He He Hu Xi Za Zhi = Zhonghua Jiehe He Huxi Zazhi = Chinese Journal of Tuberculosis and Respiratory Diseases
|October 7, 2005
PubMed
Abstract

Insights

Pulmonary surfactant associated protein A (SPA) levels significantly decrease in acute pulmonary embolism (PE) rat models. This reduction in SPA may contribute to the development of hypoxemia associated with PE.

Area of Science:

  • Pulmonary Medicine
  • Biochemistry
  • Pathophysiology

Context:

  • Acute pulmonary embolism (PE) is a critical condition affecting lung vasculature.
  • Pulmonary surfactant associated protein A (SPA) is crucial for lung function.
  • Understanding SPA's role in PE is vital for developing therapeutic strategies.

Purpose:

  • To investigate the dynamic changes in pulmonary surfactant associated protein A (SPA) expression in lung tissue during acute pulmonary embolism (PE).

Summary:

  • Male SD rats were subjected to PE induction using gelfoam microspheres.
  • Pulmonary artery pressure, heart rate, and oxygen levels were monitored.
  • RT-PCR and Western blot analyses revealed significant decreases in SPA mRNA and protein levels post-embolism.

Impact:

  • The study demonstrates a significant downregulation of SPA in acute PE.
  • Reduced SPA levels correlate with hypoxemia, suggesting a potential role in the pathophysiology of PE-induced respiratory distress.

More Related Videos

Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)07:20

Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)

Published on: September 7, 2016

Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet09:22

Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet

Published on: November 4, 2015

Related Concept Videos

Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
Pulmonary Embolism I: Introduction01:19

Pulmonary Embolism I: Introduction

A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
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.
Breathing01:05

Breathing

The process of breathing, inhaling and exhaling, involves the coordinated movement of the chest wall, the lungs, and the muscles that move them. Two muscle groups with important roles in breathing are the diaphragm, located directly below the lungs, and the intercostal muscles, which lie between the ribs. When the diaphragm contracts, it moves downward, increasing the volume of the thoracic cavity and creating more room for the lungs to expand. When the intercostal muscles contract, the ribs...