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Publication : Impact of physiological variables and genetic background on myocardial frequency-resistivity relations in the intact beating murine heart.

First Author  Reyes M Year  2006
Journal  Am J Physiol Heart Circ Physiol Volume  291
Issue  4 Pages  H1659-69
PubMed ID  16699072 Mgi Jnum  J:116438
Mgi Id  MGI:3694302 Doi  10.1152/ajpheart.00609.2005
Citation  Reyes M, et al. (2006) Impact of physiological variables and genetic background on myocardial frequency-resistivity relations in the intact beating murine heart. Am J Physiol Heart Circ Physiol 291(4):H1659-69
abstractText  Conductance measurements for generation of an instantaneous left ventricular (LV) volume signal in the mouse are limited, because the volume signal is a combination of blood and LV muscle, and only the blood signal is desired. We have developed a conductance system that operates at two simultaneous frequencies to identify and remove the myocardial contribution to the instantaneous volume signal. This system is based on the observation that myocardial resistivity varies with frequency, whereas blood resistivity does not. For calculation of LV blood volume with the dual-frequency conductance system in mice, in vivo murine myocardial resistivity was measured and combined with an analytic approach. The goals of the present study were to identify and minimize the sources of error in the measurement of myocardial resistivity to enhance the accuracy of the dual-frequency conductance system. We extended these findings to a gene-altered mouse model to determine the impact of measured myocardial resistivity on the calculation of LV pressure-volume relations. We examined the impact of temperature, timing of the measurement during the cardiac cycle, breeding strain, anisotropy, and intrameasurement and interanimal variability on the measurement of intact murine myocardial resistivity. Applying this knowledge to diabetic and nondiabetic 11- and 20- to 24-wk-old mice, we demonstrated differences in myocardial resistivity at low frequencies, enhancement of LV systolic function at 11 wk and LV dilation at 20-24 wk, and histological and electron-microscopic studies demonstrating greater glycogen deposition in the diabetic mice. This study demonstrated the accurate technique of measuring myocardial resistivity and its impact on the determination of LV pressure-volume relations in gene-altered mice.
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