Related Experiment Video

Updated: Jul 23, 2026

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

Decreased surfactant proteins in lambs with pulmonary hypertension secondary to increased blood flow

J A Gutierrez1, A J Parry, D M McMullan

  • 1Department of Pediatrics, University of California, San Francisco, California 94143, USA. jgut@itsa.ucsf.edu

American Journal of Physiology. Lung Cellular and Molecular Physiology
|October 13, 2001
PubMed

Insights

Congenital heart disease in lambs with pulmonary hypertension led to reduced surfactant proteins A and B. This finding highlights potential impacts on lung function in related infant conditions.

Area of Science:

  • Pulmonary Medicine
  • Neonatology
  • Cardiovascular Research

Background:

  • Infants with congenital heart disease (CHD) often experience pulmonary hypertension, leading to respiratory distress and infections.
  • Increased pulmonary blood flow is a common cause of pulmonary hypertension in infants with CHD.
  • Surfactant proteins are crucial for lung function, particularly in premature infants.

Purpose of the Study:

  • To investigate the impact of pulmonary hypertension, secondary to increased pulmonary blood flow, on surfactant protein expression in a lamb model.
  • To quantify changes in surfactant protein A (SP-A), SP-B, and SP-C mRNA and protein levels.

Main Methods:

  • Utilized a lamb model with surgically created aortopulmonary vascular grafts to induce pulmonary hypertension.
  • Assessed SP-A, SP-B, and SP-C mRNA and protein expression at 4 weeks of age using quantitative methods.
  • Compared expression levels in lambs with induced pulmonary hypertension to age-matched controls.

Main Results:

  • SP-A mRNA content decreased significantly to 61.4% of control values.
  • SP-A protein content showed a marked decrease to 50% of control values.
  • SP-B protein content was reduced to 74% of control values, though SP-B mRNA did not change significantly. SP-C mRNA remained unchanged.

Conclusions:

  • Increased pulmonary blood flow in a lamb model of CHD with pulmonary hypertension leads to decreased SP-A gene expression and reduced SP-A and SP-B protein levels.
  • These alterations in surfactant protein expression may contribute to the respiratory complications observed in infants with similar conditions.
  • The study provides insights into the molecular mechanisms underlying lung dysfunction in CHD-associated pulmonary hypertension.

More Related Videos

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets08:08

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Published on: May 11, 2015

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

Related Concept Videos

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...
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...
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...