Ambient Particulate Matter Affects Cardiac Recovery in a Langendorff Ischemia Model

Bagaté, Karim; Meiring, James J; Gerlofs-Nijland, Miriam E.; Cassee, Flemming R.; Wiegand, Herbert; Osornio-Vargas, Álvaro; Borm, Paul J. A.

doi:10.1080/08958370600742706

Cited by 26 publications

(8 citation statements)

References 35 publications

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“…In contrast, inhalational exposure produced a milder, more prolonged inflammatory response and reduced particle availability. Impaired LV contractility was also demonstrated ex vivo in isolated perfused hearts from normotensive rats and SHRs 4 h after the intratracheal instillation of combustion-generated fine particles or when DEPs were directly added to the perfusion buffer (3,43). Inhalational exposure to carbon black particles (Յ0.1 m) significantly decreased baseline systolic and diastolic function in senescent (28 mo old) mice; however, cardiac function was not altered when middle-aged (18 mo old) healthy mice were similarly exposed to the same particles (40).…”

Section: Discussionmentioning

confidence: 96%

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

Mahne

Chuang

Pankey

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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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.

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Section: Discussionmentioning

confidence: 96%

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

Mahne

Chuang

Pankey

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…The Langendorff cardiac perfusion model is a standardized ex vivo technique used for experimental study of the clinical relevance of myocardial infarction from an ischemia/reperfusion insult. It has also been used to investigate the mechanisms that underlie the increased risk of ischemic heart diseases induced by air pollution exposure in animals [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Differential Cardiopulmonary Effects of Size-Fractionated Ambient Particulate Matter in Mice

et al. 2010

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A growing body of evidence from epidemiological and toxicological studies provides a strong link between exposure to ambient particulate matter (PM) of varying size and increased cardiovascular and respiratory morbidity and mortality. This study was designed to evaluate the cardiopulmonary effects of ambient coarse, fine, and ultrafine particles collected in Chapel Hill, NC. Mice were exposed to each size fraction by oropharyngeal instillation. Twenty-four hours later, pulmonary inflammation was assessed by bronchoalveolar lavage and cardiac injury was measured using a Langendorff cardiac perfusion preparation. Recovery of post-ischemic left ventricular developed pressure and infarct size were measured as indeces of cardiac ischemia/reperfusion injury. Coronary flow rate was measured before, during, and after ischemia. We demonstrate that coarse PM caused the most significant pulmonary inflammatory responses. In contrast, hearts from ultrafine-exposed mice had significantly lower post-ischemic functional recovery and greater infarct size, while hearts from coarse and fine PM-exposed mice had no significant responses to ischemia/reperfusion. The coronary flow rate was significantly reduced in the ultrafine PM group. This study shows that exposure of mice to coarse PM results in significant pulmonary toxicity while ultrafine PM appears to enhance cardiac ischemia/reperfusion injury.

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“…Zinc, an essential transition divalent cation, is involved in maintaining and regulating cellular and subcellular functions of virtually all cells. Four major roles of Zn 21 have been reported: 1), it binds tightly to metalloenzymes and serves as a cofactor in gene expression and enzymatic reactions (3); 2), it is abundant in the brain, where it is localized in the presynaptic terminals, is coreleased with glutamate (4,5), and regulates neuronal excitability and synaptic plasticity (6,7); 3), it is involved in many pathological neuromodulatory events, and the accumulation of Zn 21 during and after transient global ischemia (8,9) can also affect cardiac functions (10,11); and 4), it regulates conductivity of VDCCs (12)(13)(14) and affects Ca 21 signaling.…”

Section: Introductionmentioning

confidence: 99%

Zn2+ Sensitivity of High- and Low-Voltage Activated Calcium Channels

Sun

Hui

Lee

et al. 2007

Biophysical Journal

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The essential cation zinc (Zn2+) blocks voltage-dependent calcium channels in several cell types, which exhibit different sensitivities to Zn2+. The specificity of the Zn2+ effect on voltage-dependent calcium channel subtypes has not been systematically investigated. In this study, we used a transient protein expression system to determine the Zn2+ effect on low- and high-voltage activated channels. We found that in Ba2+, the IC50 value of Zn2+ was alpha1-subunit-dependent with lowest value for CaV1.2, and highest for CaV3.1; the sensitivity of the channels to Zn2+ was approximately ranked as CaV1.2>CaV3.2>CaV2.3>CaV2.2=CaV 2.1>or=CaV3.3=CaV3.1. Although the CaV2.2 and CaV3.1 channels had similar IC50 for Zn2+ in Ba2+, the CaV2.2, but not CaV3.1 channels, had approximately 10-fold higher IC50 to Zn2+ in Ca2+. The reduced sensitivity of CaV2.2 channels to Zn2+ in Ca2+ was partially reversed by disrupting a putative EF-hand motif located external to the selectivity filter EEEE locus. Thus, our findings support the notion that the Zn2+ block, mediated by multiple mechanisms, may depend on conformational changes surrounding the alpha1 pore regions. These findings provide fundamental insights into the mechanism underlying the inhibitory effect of zinc on various Ca2+ channel subtypes.

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Ambient Particulate Matter Affects Cardiac Recovery in a Langendorff Ischemia Model

Cited by 26 publications

References 35 publications

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

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

Differential Cardiopulmonary Effects of Size-Fractionated Ambient Particulate Matter in Mice

Zn2+ Sensitivity of High- and Low-Voltage Activated Calcium Channels

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