Literature DB >> 12775560

Measurement of aortic input impedance in mice: effects of age on aortic stiffness.

Anilkumar K Reddy1, Yi-Heng Li, Thuy T Pham, Lyssa N Ochoa, Maria T Trevino, Craig J Hartley, Lloyd H Michael, Mark L Entman, George E Taffet.   

Abstract

Mice are used with increasing frequency as models of human cardiovascular diseases, but significant gaps exist in our knowledge of vascular function in the aging mouse. We determined aortic input impedance spectra, pulse wave velocity, and augmentation index in adult (8-mo-old) and old (29-mo-old) mice to determine whether arterial stiffening occurred with age in mice as it does in humans. Pressure and blood velocity signals measured simultaneously from the same location in the ascending aorta were used to determine input impedance spectra (0-10 harmonics). The first minimum of the impedance modulus occurred at the second harmonic in adult mice but shifted to the fourth harmonic in old mice. Characteristic impedance (average of 2nd-10th harmonic) was 57% higher in old mice: 471 +/- 62 vs. 299 +/- 10 (SE) dyn.s.cm-3 (P < 0.05). Pulse pressure and augmentation index, determined from the aortic pressure signals, were also higher in old mice: 42 +/- 2.2 vs. 29 +/- 4.9 mmHg (P < 0.05) and 37 +/- 5 vs. 14 +/- 2% (P < 0.005). Aortic pulse wave velocity measured from the timing of upstrokes of the Doppler velocity signals was 45% higher in old mice: 416 +/- 22 vs. 286 +/- 14 cm/s (n = 3, P < 0.01). These results reproduce age-related findings reported in humans and confirm that mice may be used as models of age-related vascular stiffening.

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Year:  2003        PMID: 12775560     DOI: 10.1152/ajpheart.00004.2003

Source DB:  PubMed          Journal:  Am J Physiol Heart Circ Physiol        ISSN: 0363-6135            Impact factor:   4.733


  34 in total

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8.  Effect of isoflurane on aortic impedance in mice.

Authors:  Anilkumar K Reddy; Khodidad Namiranian; Eric E Lloyd; Robert M Bryan; George E Taffet; Craig J Hartley
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10.  B6D2F1 Mice are a suitable model of oxidative stress-mediated impaired endothelium-dependent dilation with aging.

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