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Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
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Published on: December 10, 2021

Environmentally persistent free radicals decrease cardiac function and increase pulmonary artery pressure.

Sarah Mahne1, Gin C Chuang, Edward Pankey

  • 1Department of Pharmacology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|September 4, 2012
PubMed
Summary

Inhaling environmentally persistent free radicals (EPFRs) reduced heart function in healthy rats by impairing cardiac filling. This study highlights EPFRs as a risk factor for cardiac issues, even in non-at-risk individuals.

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Area of Science:

  • Environmental Health
  • Cardiovascular Toxicology
  • Toxicology

Background:

  • Epidemiological studies link particulate matter (PM) inhalation to cardiac events, particularly in vulnerable groups.
  • Research on PM's impact on baseline cardiac function in healthy individuals is limited.
  • Airborne PM can contain environmentally persistent free radicals (EPFRs) with redox cycling potential.

Purpose of the Study:

  • To investigate the effects of EPFR inhalation on baseline left ventricular function in healthy rats.
  • To determine if controlled EPFR exposure can impair cardiac performance in a healthy model.

Main Methods:

  • Healthy male Sprague-Dawley rats were exposed via inhalation to a model EPFR (1,2-dichlorobenzene on silica/CuO particles) or controls for 7 days.
  • Left ventricular function was assessed using pressure-volume catheters 24 hours post-exposure.
  • Cardiac function, pulmonary pressures, and biochemical markers (C-reactive protein, oxidative stress markers) were measured.

Main Results:

  • EPFR inhalation significantly decreased stroke volume, cardiac output, and stroke work.
  • Reduced end-diastolic volume and pressure were observed, indicating impaired cardiac filling.
  • EPFR exposure increased pulmonary arterial pressure, pulmonary artery hyperplasia, systemic inflammation (CRP), and cardiac oxidative stress markers (HO-1, SOD2).

Conclusions:

  • Inhalation of EPFRs, but not control silica particles, impairs baseline cardiac function in healthy rats.
  • The observed cardiac dysfunction is attributed to decreased cardiac filling, secondary to increased pulmonary resistance.
  • EPFR exposure induces systemic inflammation and oxidative stress in the heart.