scholarly journals Effects of alterations in aortic input impedance on the force-velocity-length relationship in the intact canine heart.

1979 ◽  
Vol 45 (1) ◽  
pp. 126-136 ◽  
Author(s):  
H Pouleur ◽  
J W Covell ◽  
J Ross
Keyword(s):  
Input Impedance ◽  
Canine Heart ◽  
Length Relationship ◽  
Aortic Input Impedance ◽  
Force Velocity

scholarly journals Aortic input impedance in heart failure.

Circulation ◽  
1978 ◽  
Vol 58 (3) ◽  
pp. 460-465 ◽  
Author(s):  
C J Pepine ◽  
W W Nichols ◽  
C R Conti
Keyword(s):  
Heart Failure ◽  
Input Impedance ◽  
Aortic Input Impedance

Force-Velocity-Length Relationship during Cardiac Hypertrophy

1983 ◽  
pp. 87-95 ◽  
Author(s):  
Y. Lecarpentier ◽  
P. Gastineau ◽  
P. Y. Hatt ◽  
J. L. Martin
Keyword(s):  
Cardiac Hypertrophy ◽  
Length Relationship ◽  
Force Velocity

scholarly journals Influence of joint angle on muscle fascicle dynamics and rate of torque development during isometric explosive contractions

2020 ◽  
Vol 129 (3) ◽  
pp. 569-579
Author(s):  
Robin Hager ◽  
Thomas Poulard ◽  
Antoine Nordez ◽  
Sylvain Dorel ◽  
Gaël Guilhem
Keyword(s):  
Joint Angle ◽  
Limiting Factor ◽  
Gastrocnemius Medialis ◽  
Rate Of Torque Development ◽  
Muscle Fascicle ◽  
Length Relationship ◽  
Ankle Angle ◽  
Generating Capacity ◽  
Force Velocity ◽  
Torque Development

Ankle angle influences the operating muscle fascicle lengths of gastrocnemius medialis and the rate of torque development during explosive isometric plantar flexions. The rate of torque development peaks in neutral angles where muscle fascicles shorten over the plateau of the force-length relationship. When fascicles operate over the plateau of the force-length relationship (neutral ankle positions), the force-velocity properties represent a limiting factor for the rapid force-generating capacity from 100 ms after the onset of explosive contractions.

scholarly journals Effects of Nicorandil on Aortic Input Impedance

1999 ◽  
Vol 63 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Masami Fujita ◽  
Kenji Takazawa ◽  
Nobuhiro Tanaka ◽  
Chiharu Ibukiyama
Keyword(s):  
Input Impedance ◽  
Aortic Input Impedance

Differential Effects of Isoflurane and Halothane on Aortic Input Impedance Quantified Using a Three-element Windkessel Model

1995 ◽  
Vol 83 (2) ◽  
pp. 361-373. ◽  
Author(s):  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Blood Flow ◽  
Input Impedance ◽  
Wave Reflection ◽  
Conscious State ◽  
Left Ventricular ◽  
Arterial System ◽  
Windkessel Model ◽  
Frequency Dependent ◽  
Aortic Input Impedance ◽  
Arterial Wave Reflection

Background Systemic vascular resistance (the ratio of mean aortic pressure [AP] and mean aortic blood flow [AQ]) does not completely describe left ventricular (LV) afterload because of the phasic nature of pressure and blood flow. Aortic input impedance (Zin) is an established experimental description of LV afterload that incorporates the frequency-dependent characteristics and viscoelastic properties of the arterial system. Zin is most often interpreted through an analytical model known as the three-element Windkessel. This investigation examined the effects of isoflurane, halothane, and sodium nitroprusside (SNP) on Zin. Changes in Zin were quantified using three variables derived from the Windkessel: characteristic aortic impedance (Zc), total arterial compliance (C), and total arterial resistance (R). Methods Sixteen experiments were conducted in eight dogs chronically instrumented for measurement of AP, LV pressure, maximum rate of change in left ventricular pressure, subendocardial segment length, and AQ. AP and AQ waveforms were recorded in the conscious state and after 30 min equilibration at 1.25, 1.5, and 1.75 minimum alveolar concentration (MAC) isoflurane and halothane. Zin spectra were obtained by power spectral analysis of AP and AQ waveforms and corrected for the phase responses of the transducers. Zc and R were calculated as the mean of Zin between 2 and 15 Hz and the difference between Zin at zero frequency and Zc, respectively. C was determined using the formula C = (Ad.MAP).[MAQ.(Pes-Ped)]-1, where Ad = diastolic AP area; MAP and MAQ = mean AP and mean AQ, respectively; and Pes and Ped = end-systolic and end-diastolic AP, respectively. Parameters describing the net site and magnitude of arterial wave reflection were also calculated from Zin. Eight additional dogs were studied in the conscious state before and after 15 min equilibration at three equihypotensive infusions of SNP. Results Isoflurane decreased R (3,205 +/- 315 during control to 2,340 +/- 2.19 dyn.s.cm-5 during 1.75 MAC) and increased C(0.55 +/- 0.02 during control to 0.73 +/- 0.06 ml.mmHg-1 during 1.75 MAC) in a dose-related manner. Isoflurane also increased Zc at the highest dose. Halothane increased C and Zc but did not change R. Equihypotensive doses of SNP decreased R and produced marked increases in C without changing Zc. No changes in the net site or the magnitude of arterial wave reflection were observed with isoflurane and halothane, in contrast to the findings with SNP. Conclusions The major difference between the effects of isoflurane and halothane on LV afterload derived from the Windkessel model of Zin was related to R, a property of arteriolar resistance vessels, and not to Zc or C, the mechanical characteristics of the aorta. No changes in arterial wave reflection patterns determined from Zin spectra occurred with isoflurane and halothane. These results indicate that isoflurane and halothane have no effect on frequency-dependent arterial properties.

Aortic input impedance in mitral regurgitation

1981 ◽  
Vol 47 ◽  
pp. 426
Author(s):  
Wilmer W. Nichols ◽  
Carl J. Pepine ◽  
Jawahar Mehta ◽  
Leonard G. Christie ◽  
C. Richard Conti
Keyword(s):  
Mitral Regurgitation ◽  
Input Impedance ◽  
Aortic Input Impedance

Propofol Alters Left Ventricular Afterload as Evaluated by Aortic Input Impedance in Dogs

1996 ◽  
Vol 84 (2) ◽  
pp. 368-376. ◽  
Author(s):  
Dermot Lowe ◽  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Input Impedance ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
High Dose ◽  
Left Ventricular Afterload ◽  
Arterial Resistance ◽  
Ventricular Afterload ◽  
Total Arterial Compliance ◽  
Aortic Input Impedance ◽  
Aortic Impedance

Background Systemic vascular resistance incompletely describes left ventricular afterload because of the phasic nature of arterial pressure and blood flow. Aortic input impedance is an experimental description of left ventricular afterload that incorporates the frequency- dependent characteristics and viscoelastic properties of the arterial system. The effects of propofol on aortic input impedance were examined using three variables derived from the three-element Windkessel model: characteristic aortic impedance, total arterial compliance, and total arterial resistance. Methods Eight dogs were chronically instrumented for measurement of aortic pressure, left ventricular pressure, +dP/dt, subendocardial segment length, and aortic blood flow. Systemic hemodynamics and aortic blood pressure and flow waveforms were recorded in the conscious state and after a bolus of 5 mg x kg(-1) propofol and infusion for 15 min at 25, 50 and 100 mg x kg(-1) x h(-1). Aortic input impedance spectra were generated using power spectral analysis of aortic pressure and flow waveforms corrected for the phase responses of the pressure and flow transducers. Characteristic aortic impedance, total arterial resistance, and total arterial compliance were calculated from the aortic input impedance spectrum and the aortic pressure waveform. Parameters describing the net site and magnitude or arterial wave reflection were determined from aortic impedance. Results Propofol decreased total arterial resistance (3.05 +/- 0.20 during control to 2.29 +/- 0.18 dynes x s x cm(-5) x 10(3) at the high dose) and increased total arterial compliance (0.53 +/- 0.04 during control to 1.15 +/- 0.17 ml x mmHg(-1) at the high dose) in a dose- related manner. Propofol increased characteristic aortic impedance (1.49 +/- 0.15 during control to 2.20 +/- 0.20 dynes x s x cm(-5) x 10(2) at the high dose). The net site and the magnitude of arterial wave reflection were unchanged by the propofol. Conclusions In chronically instrumented dogs, propofol decreased total arterial resistance, a property of arteriolar resistance vessels, consistent with the known actions of this drug on systemic vascular resistance. Propofol also increased total arterial compliance and characteristic aortic impedance, indicating that this anesthetic affects the mechanical properties of the aorta. Propofol had no effect on arterial wave reflection patterns. The results indicate that propofol reduces left ventricular afterload via decreases in peripheral resistance and increases in arterial compliance.

scholarly journals Aortic input impedance in normal man: relationship to pressure wave forms.

Circulation ◽  
1980 ◽  
Vol 62 (1) ◽  
pp. 105-116 ◽  
Author(s):  
J P Murgo ◽  
N Westerhof ◽  
J P Giolma ◽  
S A Altobelli
Keyword(s):  
Input Impedance ◽  
Pressure Wave ◽  
Aortic Input Impedance ◽  
Wave Forms ◽  
Normal Man
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