Article: article from journal or magazin.
Effects of an aging vascular model on healthy and diseased hearts.
American Journal of Physiology. Heart and Circulatory Physiology
Publication types: Journal Article
The vitamin D(3) and nicotine (VDN) model is a model of isolated systolic hypertension (ISH) due to arterial calcification raising arterial stiffness and vascular impedance similar to an aged and stiffened arterial tree. We therefore analyzed the impact of this aging model on normal and diseased hearts with myocardial infarction (MI). Wistar rats were treated with VDN (n = 9), subjected to MI by coronary ligation (n = 10), or subjected to a combination of both MI and VDN treatment (VDN/MI, n = 14). A sham-treated group served as control (Ctrl, n = 10). Transthoracic echocardiography was performed every 2 wk, whereas invasive indexes were obtained at week 8 before death. Calcium, collagen, and protein contents were measured in the heart and the aorta. Systolic blood pressure, pulse pressure, thoracic aortic calcium, and end-systolic elastance as an index of myocardial contractility were highest in the aging model group compared with MI and Ctrl groups (P(VDN) < 0.05, 2-way ANOVA). Left ventricular wall stress and brain natriuretic peptide (P(VDNxMI) = not significant) were highest, while ejection fraction, stroke volume, and cardiac output were lowest in the combined group versus all other groups (P(VDNxMI) < 0.05). The combination of ISH due to this aging model and MI demonstrates significant alterations in cardiac function. This model mimics several clinical phenomena of cardiovascular aging and may thus serve to further study novel therapies.
Aging/physiology, Animals, Cardiomyopathies/chemically induced, Cardiomyopathies/physiopathology, Cardiovascular System/physiopathology, Cholecalciferol, Disease Models, Animal, Hypertension/chemically induced, Hypertension/physiopathology, Male, Myocardial Contraction/physiology, Myocardial Infarction/chemically induced, Myocardial Infarction/physiopathology, Nicotine, Rats, Rats, Wistar, Stroke Volume/physiology, Ventricular Dysfunction, Left/chemically induced, Ventricular Dysfunction, Left/physiopathology
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