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

• Published in: American journal of physiology. Heart and circulatory physiology 2005-03, Vol.288 (3), p.H1157-H1164
• Main Authors: Segers, Patrick, Georgakopoulos, Dimitrios, Afanasyeva, Marina, Champion, Hunter C, Judge, Daniel P, Millar, Huntly D, Verdonck, Pascal, Kass, David A, Stergiopulos, Nikos, Westerhof, Nico
• Format: Article
• Language: English
• Subjects: Animals; Aorta - physiology; Blood Pressure - physiology; Cardiac Volume - physiology; Catheterization - methods; Female; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Models, Animal; Vena Cava, Inferior - physiology; Ventricular Function, Left - physiology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00414.2004

1 Hydraulics Laboratory, Institute Biomedical Technology, Ghent University, Gent, Belgium; Division of Cardiology, 2 Department of Medicine, and 3 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; 4 Millar Instruments, Houston, Texas; 5 Laboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology (Écóle Polytechnique Fédérale de Lausanne), Lausanne, Switzerland; and 6 Laboratory 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 Address for reprint requests and other