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Journal ArticleDOI

Measurement of aortic input impedance in rats

TLDR
Three methods of estimating characteristic impedance from the impedance spectra were evaluated and found to produce comparable results at baseline and following pharmacological elevation of blood pressure with graded methoxamine infusion.
Abstract
Measurement of aortic input impedance in the rat is complicated by a high basal heart rate but is possible if appropriate compensation is made for frequency-dependent errors in modulus and phase resulting from analog filters in the equipment and from nonalignment of pressure and flow sensors. Because input impedance is a complex quantity, accurate values for both phase and modulus are required before meaningful interpretation of the data can be made. We measured aortic pressure and electromagnetic ascending aortic blood flow in mature, ether-anesthetized, open-chest male Wistar rats. Pressure and flow waveforms were averaged in the time domain and converted to Fourier series. Flow moduli were corrected for the measured frequency response of the flowmeter. Phase spectra were corrected by the classic frequency-domain and two new time-domain methods. Compensation for instrumentation errors was assessed at two different flowmeter filter settings in five animals. Reproducibility, variability, and the effects of vasoconstriction were assessed in 43 animals. Three methods of estimating characteristic impedance from the impedance spectra were evaluated and found to produce comparable results at baseline and following pharmacological elevation of blood pressure with graded methoxamine infusion. Physiologically equivalent values for phase, as assessed by comparing oscillatory power calculated from the impedance spectra, were obtained with each of the phase-correction techniques. The new time-domain methods facilitate the assessment of aortic input impedance in this small animal model because they do not require measurement of the spatial separation between pressure and flow transducers and pulse wave velocity in the proximal aorta.

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Journal ArticleDOI

Changes in Arterial Stiffness and Wave Reflection With Advancing Age in Healthy Men and Women: The Framingham Heart Study

TL;DR: In this healthy cohort with a minimal burden of cardiovascular disease risk factors, an age-related increase in aortic stiffness was associated with increasing forward wave amplitude and pulse pressure and reversal of the arterial stiffness gradient, which may facilitate forward transmission of potentially deleterious pressure pulsations into the periphery.
Journal ArticleDOI

Pulsatile Hemodynamics in Congestive Heart Failure

TL;DR: CHF subjects have elevated central pulsatile load (Zc), which is not apparent in global measures such as augmentation index or TAC, possibly because of contrasting changes in central and peripheral conduit vessels.
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Pulmonary Vascular Wall Stiffness: An Important Contributor to the Increased Right Ventricular Afterload with Pulmonary Hypertension:

TL;DR: The current state of knowledge of the causes and consequences of pulmonary arterial stiffening in PH and its impact on RV function is reviewed and the relationship between PA stiffening and RV dysfunction is investigated.
Journal ArticleDOI

Influence of Aortic Impedance on the Development of Pressure-Overload Left Ventricular Hypertrophy in Rats

TL;DR: The sustained early systolic loading due to the increase in characteristic impedance was accompanied by less concentric, reduced hypertrophy, whereas the sustained late syStolic loadingDue to the augmented arterial wave reflection was accompany by concentric and adequatehypertrophy.
Journal ArticleDOI

Cardiac consequences of prolonged exposure to an isolated increase in aortic stiffness

TL;DR: Three months' exposure to increased aortic stiffness in VDN rats induced LV hypertrophy with moderate interstitial fibrosis and a shift in the MHC-isoform pattern, which maintains LV performance.
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