title: Impact of physiological variables and genetic background on myocardial frequency-resistivity relations in the intact beating murine heart.
abstract: 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.
authors.affiliation: Univ. of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900, USA.
authors.forename: Maricela
authors.initials: M
authors.lastname: Reyes
authors.forename: Mark E
authors.initials: ME
authors.lastname: Steinhelper
authors.forename: Jorge A
authors.initials: JA
authors.lastname: Alvarez
authors.forename: Daniel
authors.initials: D
authors.lastname: Escobedo
authors.forename: John
authors.initials: J
authors.lastname: Pearce
authors.forename: Jonathan W
authors.initials: JW
authors.lastname: Valvano
authors.forename: Brad H
authors.initials: BH
authors.lastname: Pollock
authors.forename: Chia-Ling
authors.initials: CL
authors.lastname: Wei
authors.forename: Anil
authors.initials: A
authors.lastname: Kottam
authors.forename: David
authors.initials: D
authors.lastname: Altman
authors.forename: Steven
authors.initials: S
authors.lastname: Bailey
authors.forename: Sharon
authors.initials: S
authors.lastname: Thomsen
authors.forename: Shuko
authors.initials: S
authors.lastname: Lee
authors.forename: James T
authors.initials: JT
authors.lastname: Colston
authors.forename: Jung Hwan
authors.initials: JH
authors.lastname: Oh
authors.forename: Gregory L
authors.initials: GL
authors.lastname: Freeman
authors.forename: Marc D
authors.initials: MD
authors.lastname: Feldman
mesh_terms: D000818:Animals; D001810:Blood Volume / Q000235:genetics / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D004594:Electrophysiology; D005260:Female; D006321:Heart / Q000502:physiology*; D006329:Heart Conduction System / Q000502:physiology*; D006339:Heart Rate / Q000235:genetics / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009200:Myocardial Contraction / Q000235:genetics / Q000502:physiology*; D009206:Myocardium / Q000473:pathology; D013696:Temperature; D014655:Vascular Resistance / Q000235:genetics / Q000502:physiology*; D016277:Ventricular Function, Left / Q000235:genetics / Q000502:physiology*