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1 Laboratory of Haemodynamics and Cardiovascular Technology, EPFL, Lausanne, Switzerland; Department of Cardiovascular Surgery, CHUV, Lausanne, Switzerland
2 Laboratory of Haemodynamics and Cardiovascular Technology, EPFL, Lausanne, Switzerland
3 Department of Cardiology,, CHUV, Lausanne, Switzerland
4 Hydraulics Laboratory, Institute of Biomedical Technology,, Ghent University, Gent, GE, Belgium
5 , Pharmacy Faculty,, Pharmacology Laboratory, Nancy, France
* To whom correspondence should be addressed. E-mail: david.jegger{at}epfl.ch.
Objective: Rodent models of isolated systolic hypertension (ISH) are rare. One exception is the vitamin D3 and nicotine (VDN) model, in which arterial calcification raises arterial stiffness and vascular impedance. Although several aspects of the effects of VDN treatment on arterial or cardiac hemodynamics have been investigated, a complete analysis of the effect of VDN on ventricular-arterial interaction has not yet been performed.
Methods: Wistar rats were treated with VDN (VDN group, n=9) and a control group (CTRL, n=10) was included without the VDN treatment. At week 8, invasive indexes of cardiac function were obtained using a conductance catheter. At the same time, aortic pressure and flow were measured to derive vascular impedance and characterize ventricular-vascular interaction.
Results: VDN caused significant increases in systolic (138±6 mmHg vs. 116±13 mmHg, p<0.01; mean ± stdev) and pulse pressures (42±10 mmHg vs. 26±4 mmHg, p<0.01) with respect to control, whereas diastolic pressure, stroke volume and cardiac output remained unaltered. Total arterial compliance decreased (0.12±0.08 ml/mmHg vs. 0.21±0.04 ml/mmHg in control, p<0.05) and pulse wave velocity increased significantly (8.8±2.5 m/s vs. 5.1±2.0 m/s in control, p<0.05). The arterial elastance rose significantly in the VDN group (p<0.05). Preload recruitable stroke work and end-systolic elastance were both elevated in the VDN group thus decreasing the ratio of arterial elastance over end-systolic elastance and augmenting efficiency. 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 mmHg vs. 8.4±1.0 mmHg in control, p<0.05).
Conclusions: We studied ventricular-arterial coupling in a VDN-induced rat model of reduced arterial compliance. The VDN treatment lead 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. The VDN model may thus prove to be a useful model to study the patho-physiological effects of increased arterial stiffness.
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