TY - CHAP M1 - Book, Section TI - Toxic Responses of the Heart and Vascular System A1 - James Kang, Y. A2 - Klaassen, Curtis D. A2 - Watkins III, John B. PY - 2015 T2 - Casarett & Doull’s Essentials of Toxicology, 3e AB - Typical chemical-induced disturbances in cardiac function consist of effects on heart rate (chronotropic), contractility (inotropic), conductivity (dromotropic), and/or excitability (bathmotropic).Cardiomyopathy includes morphologic and functional alterations induced by toxic exposure, leading to decreased cardiac output and peripheral tissue hypoperfusion.Concentric cardiac hypertrophy is an increased size of cardiac myocytes in which new contractile-protein units are assembled in parallel, resulting in a relative increase in the width of individual cardiac myocytes.Eccentric cardiac hypertrophy is an increased size of cardiac myocytes in which new contractile-protein units are assembled in series, resulting in a relatively greater increase in the length than in the width of individual myocytes.Heart failure is the inability of the heart to maintain cardiac output sufficient to meet the metabolic and oxygen demands of peripheral tissues, including changes in systolic and diastolic function that reflect specific alterations in ventricular function and abnormalities in a variety of subcellular processes.Acute cardiac toxicity occurs after a single exposure to a high dose of cardiotoxic chemicals and may be manifested by arrhythmia and can involve apoptosis.Chronic cardiac toxicity, which results from long-term exposure to chemicals, is often manifested by cardiac hypertrophy and the transition to heart failure.Any xenobiotic that disrupts ion movement or homeostasis may induce a cardiotoxic reaction composed principally of disturbances in heart rhythm.All toxicants absorbed into the circulatory system contact vascular cells before reaching other sites in the body.Common mechanisms of vascular toxicity include (1) alterations in membrane structure and function, (2) redox stress, (3) vessel-specific bioactivation of protoxicants, and (4) preferential accumulation of the active toxin in vascular cells. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accesspharmacy.mhmedical.com/content.aspx?aid=1113950911 ER -