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This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1157    most recent 00414.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (17) Citing Articles via Google Scholar Google Scholar Articles by Segers, P. Articles by Westerhof, N. Search for Related Content PubMed PubMed Citation Articles by Segers, P. Articles by Westerhof, N.

Conductance catheter-based assessment of arterial input impedance, arterial function, and ventricular-vascular interaction in mice

¹Hydraulics Laboratory, Institute Biomedical Technology, Ghent University, Gent, Belgium; Division of Cardiology, ²Department of Medicine, and ³Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; ⁴Millar Instruments, Houston, Texas; ⁵Laboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology (Écóle Polytechnique Fédérale de Lausanne), Lausanne, Switzerland; and ⁶Laboratory for Physiology, ICaR-VU, Vrije Universiteit Medical Center, Amsterdam, Netherlands

Submitted 13 May 2004 ; accepted in final form 19 October 2004

Global assessment of both cardiac and arterial function is important for a meaningful interpretation of pathophysiological changes in animal models of cardiovascular disease. We simultaneously acquired left ventricular (LV) and aortic pressure and LV volume (V_LV) in 17 open-chest anesthetized mice (26.7 ± 3.2g) during steady-state (BL) and caval vein occlusion (VCO) using a 1.4-Fr dual-pressure conductance catheter and in a subgroup of eight animals during aortic occlusion (AOO). Aortic flow was obtained from numerical differentiation of V_LV. AOO increased input impedance (Z_in) for the first two harmonics, increased characteristic impedance (0.025 ± 0.007 to 0.040 ± 0.011 mmHg·µl^–1·s, P < 0.05), and shifted the minimum in Z_in from the third to the sixth harmonic. For all conditions, the Z_in could be well represented by a four-element windkessel model. The augmentation index increased from 116.7 ± 7.8% to 145.9 ± 19.5% (P < 0.01) as well as estimated pulse-wave velocity (3.50 ± 0.94 to 5.95 ± 1.62 m/s, P < 0.05) and arterial elastance (E_a, 4.46 ± 1.62 to 6.02 ± 1.43 mmHg/µl, P < 0.01). AOO altered the maximal slope (E_max, 3.23 ± 1.02 to 5.53 ± 1.53 mmHg/µl, P < 0.05) and intercept (–19.9 ± 8.6 to 1.62 ± 13.51 µl, P < 0.01) of the end-systolic pressure-volume relation but not E_a/E_max (1.44 ± 0.43 to 1.21 ± 0.37, not significant). We conclude that simultaneous acquisition of Z_in and arterial function parameters in the mouse, based solely on conductance catheter measurements, is feasible. We obtained an anticipated response of Z_in and arterial function parameters following VCO and AOO, demonstrating the sensitivity of the measuring technique to induced physiological alterations in murine hemodynamics.

hemodynamics; augmentation index; windkessel; arterial stiffness; compliance; ventriculovascular coupling

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