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Your Environment. Your Health.

Publication Detail

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

Authors: Mahne, Sarah; Chuang, Gin C; Pankey, Edward; Kiruri, Lucy; Kadowitz, Philip J; Dellinger, Barry; Varner, Kurt J

Published In Am J Physiol Heart Circ Physiol, (2012 Nov 01)

Abstract: Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.

PubMed ID: 22942180 Exiting the NIEHS site

MeSH Terms: Administration, Inhalation; Animals; Blood Pressure/drug effects*; Blood Pressure/physiology; C-Reactive Protein/metabolism; Cardiac Output/drug effects; Cardiac Output/physiology; Chlorobenzenes/administration & dosage; Chlorobenzenes/pharmacology*; Free Radicals/administration & dosage; Free Radicals/pharmacology*; Heart/drug effects*; Heart/physiology; Male; Models, Animal; Particulate Matter/administration & dosage; Particulate Matter/pharmacology; Pulmonary Artery/drug effects*; Pulmonary Artery/physiology; Rats; Rats, Sprague-Dawley; Stroke Volume/drug effects; Stroke Volume/physiology; Ventricular Function, Left/drug effects; Ventricular Function, Left/physiology

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