Environmentally persistent free radicals compromise left ventricular function during ischemia/reperfusion injury

Area of Science:

• Environmental Health
• Cardiovascular Toxicology
• Free Radical Chemistry

Background:

• Airborne particulate matter (PM) exposure is associated with increased mortality from myocardial ischemia.
• Particulate matter contains environmentally persistent free radicals (EPFRs) capable of redox cycling.

Purpose of the Study:

• To investigate if exposure to the EPFR DCB230 increases cardiac vulnerability to myocardial ischemia-reperfusion (MI/R) injury.
• To assess the impact of EPFR inhalation on left ventricular (LV) function and infarct size after MI/R.

Main Methods:

• Rats were exposed to DCB230 or vehicle via inhalation for 7 days.
• Myocardial ischemia-reperfusion (MI/R) or sham MI/R was induced 24 hours after the final exposure.
• Left ventricular function and infarct size were evaluated after 1 or 7 days of reperfusion.

Main Results:

• DCB230 exposure significantly reduced cardiac output, stroke volume, and stroke work in MI/R rats.
• EPFR exposure prevented the compensatory increase in preload-recruitable stroke work (contractility).
• LV function deficits from DCB230 exposure resolved within 8 days; infarct size was unaffected.

Conclusions:

• Inhalation of EPFRs exacerbates cardiac dysfunction following MI/R injury.
• EPFRs compromise cardiac function during MI/R, potentially explaining the link between PM and MI/R mortality.
• EPFRs increase cardiac vulnerability to ischemia-reperfusion injury without altering infarct size.