Particulate matter inhalation exacerbates cardiopulmonary injury in a rat model of isoproterenol-induced cardiomyopathy

Autor:	William H. Rowan, Wayne E. Cascio, Aimen K. Farraj, William P. Watkinson, Mehdi S. Hazari, Daniel L. Costa, Alex P. Carll, Najwa Haykal-Coates, Darrell W. Winsett, Allen D. Ledbetter, Abraham Nyska
Rok vydání:	2010
Předmět:	Male medicine.medical_specialty Heart disease Injections Subcutaneous Health Toxicology and Mutagenesis Cardiomyopathy Toxicology Rats Inbred SHR Internal medicine Heart rate Animals Telemetry Medicine Heart rate variability Lung Heart Failure Inhalation exposure Air Pollutants Inhalation Exposure L-Lactate Dehydrogenase Inhalation business.industry Myocardium Hemodynamics Isoproterenol Drug Synergism Heart Organ Size Adrenergic beta-Agonists medicine.disease Rats Disease Models Animal Heart failure Breathing Cardiology Particulate Matter Cardiomyopathies Lipoproteins HDL business
Zdroj:	Inhalation Toxicology. 22:355-368
ISSN:	1091-7691 0895-8378
DOI:	10.3109/08958370903365692
Popis:	Ambient particulate matter (PM) exposure is linked to cardiovascular events and death, especially among individuals with heart disease. A model of toxic cardiomyopathy was developed in Spontaneously Hypertensive Heart Failure (SHHF) rats to explore potential mechanisms. Rats were infused with isoproterenol (ISO; 2.5 mg/kg/day subcutaneous [sc]), a beta-adrenergic agonist, for 28 days and subsequently exposed to PM by inhalation. ISO induced tachycardia and hypotension throughout treatment followed by postinfusion decrements in heart rate, contractility, and blood pressures (systolic, diastolic, pulse), and fibrotic cardiomyopathy. Changes in heart rate and heart rate variability (HRV) 17 days after ISO cessation indicated parasympathetic dominance with concomitantly altered ventilation. Rats were subsequently exposed to filtered air or Harvard Particle 12 (HP12) (12 mg/m(3))--a metal-rich oil combustion-derived PM--at 18 and 19 days (4 h/day) after ISO infusion via nose-only inhalation to determine if cardio-impaired rats were more responsive to the effects of PM exposure. Inhalation of PM among ISO-pretreated rats significantly increased pulmonary lactate dehydrogenase, serum high-density lipoprotein (HDL) cholesterol, and heart-to-body mass ratio. PM exposure increased the number of ISO-pretreated rats that experienced bradyarrhythmic events, which occurred concomitantly with acute alterations of HRV. PM, however, did not significantly affect mean HRV in the ISO- or saline-pretreated groups. In summary, subchronic ISO treatment elicited some pathophysiologic and histopathological features of heart failure, including cardiomyopathy. The enhanced sensitivity to PM exposure in SHHF rats with ISO-accelerated cardiomyopathy suggests that this model may be useful for elucidating the mechanisms by which PM exposure exacerbates heart disease.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6ab1cc9e29a4f4cbe3f6ed9e04d20023 https://doi.org/10.3109/08958370903365692 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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