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Am J Physiol Heart Circ Physiol (December 16, 2004). doi:10.1152/ajpheart.00414.2004
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Submitted on May 13, 2004
Accepted on October 19, 2004

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

Patrick Segers1*, Dimitrios Georgakopoulos2, Marina Afanasyeva3, Hunter C Champion2, Daniel P Judge2, Huntley D Millar4, Pascal R Verdonck1, David A Kass2, Nikos Stergiopulos5, and Nico Westerhof6

1 Hydraulics Laboratory, Institute Biomedical Technology, Ghent University, Gent, Belgium
2 Department of Medicine, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
3 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MS, USA
4 Millar Instruments, Houston, TX, USA
5 Laboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology (EPFL), Lausanne, Switzerland
6 Laboratory for Physiology, ICaR-VU, VU University Medical Center, Amsterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: patrick.segers{at}ugent.be.

Global assessment of both cardiac and arterial function is important for a meaningful interpretation of pathophysiologic changes in animal models of cardiovascular disease. We simultaneously acquired left ventricular (LV) and aortic pressure and LV volume (VLV) 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 8 animals during aortic occlusion (AOO). Aortic flow was obtained from numerical differentiation of VLV. AOO increased input impedance (Zin) for the first 2 harmonics, characteristic impedance (0.025±0.007 to 0.040±0.011mmHg/(µl/s), P<0.05), and shifted the minimum in Zin from the 3rd to the 6th harmonic. For all conditions, the input impedance could be well represented by a 4-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, Ea (4.46±1.62 to 6.02±1.43 mmHg/µl, P<0.01). AOO altered the slope (Emax, 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 PV relation, but not Ea/Emax (1.44±0.43 to 1.21±0.37, NS). We conclude that simultaneous acquisition of Zin and arterial function parameters in the mouse, based solely on conductance catheter measurements, is feasible. We obtained an anticipated response of Zin and arterial function parameters following VCO and AOO, demonstrating the sensitivity of the measuring technique to induced physiological alterations in murine hemodynamics.




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