Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress, vagal dominance, arrhythmia and pulmonary inflammation in heart failure-prone rats

Abstract

Acute exposure to ambient fine particulate matter (PM2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiologic events precipitating these outcomes remain poorly understood but may involve inflammation, oxidative stress, arrhythmia, and autonomic nervous system imbalance. Cardiomyopathy results from cardiac injury, is the leading cause of heart failure, and can be induced in heart failure-prone rats through sub-chronic infusion of isoproterenol (ISO). To test whether cardiomyopathy confers susceptibility to inhaled PM2.5 and can elucidate potential mechanisms, we investigated the cardiophysiologic, ventilatory, inflammatory, and oxidative effects of a single nose-only inhalation of a metal-rich PM2.5 (580 μg/m3, 4h) in ISO-pretreated (35 days * 1.0 mg/kg/day sc) rats. During the 5 days post-treatment, ISO-treated rats had decreased HR and BP and increased pre-ejection period (PEP, an inverse correlate of contractility) relative to saline-treated rats. Before inhalation exposure, ISO-pretreated rats had increased PR and ventricular repolarization time (QT) and heterogeneity (Tp-Te). Relative to clean air, PM2.5 further prolonged PR-interval and decreased systolic BP during inhalation exposure; increased tidal volume, expiratory time, heart rate variability (HRV) parameters of parasympathetic tone, and atrioventricular block arrhythmias over the hours post-exposure; increased pulmonary neutrophils, macrophages, and total antioxidant status one day post-exposure; and decreased pulmonary glutathione peroxidase 8 weeks after exposure, with all effects occurring exclusively in ISO-pretreated rats but not saline-pretreated rats. Ultimately, our findings indicate that cardiomyopathy confers susceptibility to the oxidative, inflammatory, ventilatory, autonomic, and arrhythmogenic effects of acute PM2.5 inhalation.

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

“…Likewise, PEPs increased spontaneous ventricular premature beats at both 2 days and 5 weeks after the 21-day exposure, complementing epidemiologic associations between PM exposure and spontaneous ventricular arrhythmia [81,[88][89][90][91] and sudden cardiac arrest [92,93]. Interestingly, aerosol exposures in noninvasive rat models of CVD typically provoke spontaneous atrioventricular block arrhythmias [45,86,[94][95][96][97][98], which differ from the premature ventricular ectopy that predominates with PM exposure in humans. Yet, rodent models of surgical myocardial infarction [99][100][101] or genetic dilated fibrotic cardiomyopathy [102] have more consistently demonstrated tachyarrhythmias with PM exposures.…”

“…ECG waveforms were analyzed with ecgAuto, v3.3 (Emka Technologies, Paris, France) for mean RR intervals, HRV, and arrhythmia as we have previously described [86,94]. A library of 224 manually marked representative PQRST complexes was used to identify beat landmarks for ECG analyses according to previously described criteria [86].…”

Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System

“…ISO rebel in rats causes quite a lot of physiological, pathological and functional changes in the myocardium, resembling the set of symptoms of human myocardial [55][56][57][58]; hence, this model has been extensively in a job to explore and get rid of luminosity on mechanisms and treatment of myocardial necrosis. Myocardial infarction is related to various deleterious symptoms or conditions, which led to damage the cardiac tissues and showed abnormality in the membrane-bound protective guards present in the myocardium.…”

TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

“…Additionally, increases in vagal tone have been associated with adverse cardiovascular events in type II diabetics (Eguchi et al, 2010), and linked with increased mortality in heart failure patients and the elderly (de Bruyne et al, 1999; Stein et al, 2005). With regard to the animal models, we have consistently shown that exposure to different types of air pollutants such as residual oil fly ash (Carll et al, 2015; Farraj et al, 2011), diesel exhaust (Carll et al, 2013; Hazari et al, 2011), ozone (Farraj et al, 2012) and acrolein (Hazari et al, 2014) all lead to an increase in HRV in rodent models. This is not entirely surprising given increased HRV, and in particular RMSSD and HF, indicate parasympathetic modulation which is a well-characterized reflex response to airway sensory activation (Lee and Pisarri, 2001).…”