Title: Environmentally persistent free radicals compromise left ventricular function during ischemia/reperfusion injury.
Authors: Burn, Brendan R; Varner, Kurt J
Published In Am J Physiol Heart Circ Physiol, (2015 May 01)
Abstract: Increases in airborne particulate matter (PM) are linked to increased mortality from myocardial ischemia. PM contains environmentally persistent free radicals (EPFRs) that form as halogenated hydrocarbons chemisorb to transition metal oxide-coated particles, and are capable of sustained redox cycling. We hypothesized that exposure to the EPFR DCB230 would increase cardiac vulnerability to subsequent myocardial ischemia-reperfusion (MI/R) injury. Rats were exposed to DCB230 or vehicle via nose-only inhalation (230 μg max/day) over 30 min/day for 7 days. MI/R or sham MI/R (sham) was initiated 24 h after the final exposure. Following 1 or 7 days of reperfusion, left ventricular (LV) function was assessed and infarct size measured. In vehicle-exposed rats, MI/R injury did not significantly reduce cardiac output (CO), stroke volume (SV), stroke work (SW), end-diastolic volume (EDV), or end-systolic volume (ESV) after 1 day of reperfusion, despite significant reductions in end-systolic pressure (ESP). Preload-recruitable SW (PRSW; contractility) was elevated, presumably to maintain LV function. MI/R 1-day rats exposed to DCB230 also had similarly reduced ESP. Compared with vehicle controls, CO, SV, and SW were significantly reduced in DCB230-exposed MI/R 1-day rats; moreover, PRSW did not increase. DCB230's effects on LV function dissipated within 8 days of exposure. These data show that inhalation of EPFRs can exacerbate the deficits in LV function produced by subsequent MI/R injury. Infarct size was not different between the MI/R groups. We conclude that inhalation of EPFRs can compromise cardiac function during MI/R injury and may help to explain the link between PM and MI/R-related mortality.
PubMed ID: 25681431
MeSH Terms: Animals; Disease Models, Animal; Free Radicals/toxicity*; Inhalation Exposure; Male; Myocardial Infarction/chemically induced; Myocardial Infarction/etiology*; Myocardial Infarction/metabolism; Myocardial Infarction/pathology; Myocardial Infarction/physiopathology; Myocardial Reperfusion Injury/chemically induced; Myocardial Reperfusion Injury/etiology*; Myocardial Reperfusion Injury/metabolism; Myocardial Reperfusion Injury/pathology; Myocardial Reperfusion Injury/physiopathology; Myocardium/metabolism; Myocardium/pathology; Oxidative Stress/drug effects; Particle Size; Particulate Matter/toxicity*; Rats, Sprague-Dawley; Risk Assessment; Risk Factors; Stroke Volume/drug effects; Time Factors; Ventricular Dysfunction, Left/chemically induced; Ventricular Dysfunction, Left/etiology*; Ventricular Dysfunction, Left/metabolism; Ventricular Dysfunction, Left/pathology; Ventricular Dysfunction, Left/physiopathology; Ventricular Function, Left/drug effects*; Ventricular Pressure/drug effects