title: Ventricular-arterial coupling in a rat model of reduced arterial compliance provoked by hypervitaminosis D and nicotine.
abstract: The vitamin D(3) 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.
authors.affiliation: Ecole Polytechnique Fédérale de Lausanne, Laboratory of Hemodynamics and Cardiovascular Technology, CH-1015 Lausanne, Switzerland. David.Jegger@epfl.ch
authors.forename: David
authors.initials: D
authors.lastname: Jegger
authors.forename: Rafaela
authors.initials: R
authors.lastname: da Silva
authors.forename: Xavier
authors.initials: X
authors.lastname: Jeanrenaud
authors.forename: Mohammad
authors.initials: M
authors.lastname: Nasratullah
authors.forename: Hendrik
authors.initials: H
authors.lastname: Tevaearai
authors.forename: Ludwig K
authors.initials: LK
authors.lastname: von Segesser
authors.forename: Patrick
authors.initials: P
authors.lastname: Segers
authors.forename: Virginie
authors.initials: V
authors.lastname: Gaillard
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Atkinson
authors.forename: Isabelle
authors.initials: I
authors.lastname: Lartaud
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Stergiopulo
mesh_terms: D000818:Animals; D002306:Cardiac Volume / Q000187:drug effects* / Q000502:physiology; D002762:Cholecalciferol / Q000494:pharmacology*; D003187:Compliance; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004548:Elasticity / Q000187:drug effects; D005731:Ganglionic Stimulants / Q000494:pharmacology*; D006352:Heart Ventricles / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008955:Models, Cardiovascular; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D016276:Ventricular Function
chemical_list: D005731:Ganglionic Stimulants; D002762:Cholecalciferol; D009538:Nicotine