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Ventricular-arterial coupling in a rat model of reduced arterial compliance provoked by hypervitaminosis D and nicotine

¹Laboratory of Hemodynamics and Cardiovascular Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne; ²Department of Cardiovascular Surgery, Centre Hospitalière Universitaire Vardois, Lausanne; ⁴Department of Cardiovascular Surgery, Inselspital, Bern; ³Department of Cardiology, Centre Hospitalière Universitaire, Vardois, Lausanne, Switzerland; ⁶Pharmacy Faculty, Pharmacology Laboratory, Henri Poincaré University, Nancy, France; and ⁵Hydraulics Laboratory, Institute of Biomedical Technology, Ghent University, Gent, Belgium

Submitted 23 January 2006 ; accepted in final form 6 May 2006

The vitamin D₃ and nicotine (VDN) model is one of isolated systolic hypertension (ISH) in which arterial calcification raises arterial stiffness and vascular impedance. The effects of VDN treatment on arterial and cardiac hemodynamics have been investigated; however, a complete analysis of ventricular-arterial interaction is lacking. Wistar rats were treated with VDN (VDN group, n = 9), and a control group (n = 10) was included without the VDN. At week 8, invasive indexes of cardiac function were obtained using a conductance catheter. Simultaneously, aortic pressure and flow were measured to derive vascular impedance and characterize ventricular-vascular interaction. VDN caused significant increases in systolic (138 ± 6 vs. 116 ± 13 mmHg, P < 0.01) and pulse (42 ± 10 vs. 26 ± 4 mmHg, P < 0.01) pressures with respect to control. Total arterial compliance decreased (0.12 ± 0.08 vs. 0.21 ± 0.04 ml/mmHg in control, P < 0.05), and pulse wave velocity increased significantly (8.8 ± 2.5 vs. 5.1 ± 2.0 m/s in control, P < 0.05). The arterial elastance and end-systolic elastance rose significantly in the VDN group (P < 0.05). Wave reflection was augmented in the VDN group, as reflected by the increase in the wave reflection coefficient (0.63 ± 0.06 vs. 0.52 ± 0.05 in control, P < 0.05) and the amplitude of the reflected pressure wave (13.3 ± 3.1 vs. 8.4 ± 1.0 mmHg in control, P < 0.05). We studied ventricular-arterial coupling in a VDN-induced rat model of reduced arterial compliance. The VDN treatment led to development of ISH and provoked alterations in cardiac function, arterial impedance, arterial function, and ventricular-arterial interaction, which in many aspects are similar to effects of an aged and stiffened arterial tree.

blood flow; calcium; hypertension; hemodynamics; ventricular function

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