scholarly journals Variable Unstressed Volume Keeps Normal Distributions of Canine Left Ventricular Contractility and Total Mechanical Energy under Atrial Fibrillation

2005 ◽  
Vol 55 (5) ◽  
pp. 255-264 ◽  
Author(s):  
Satoshi Mohri ◽  
Juichiro Shimizu ◽  
Haruo Ito ◽  
Hiroki Yamaguchi ◽  
Shunji Sano ◽  
...  
1997 ◽  
Vol 272 (6) ◽  
pp. H2671-H2678 ◽  
Author(s):  
H. Tachibana ◽  
M. Takaki ◽  
S. Lee ◽  
H. Ito ◽  
H. Yamaguchi ◽  
...  

We recorded a series of ejecting left ventricular (LV) pressure (P)-volume (V) loops of in situ rat hearts during a gradual ascending aortic occlusion. The end-systolic (ES) P-V relationship (ESPVR) was upward convex curvilinear regardless of LV contractility. The ESPVR was shifted upward in an enhanced contractility by dobutamine and downward in a depressed contractility by propranolol; ESP at a midrange V of 0.1 ml/g LV on each ESPVR increased from 131 +/- 11 to 192 +/- 17 mmHg and decreased from 136 +/- 10 to 110 +/- 7 mmHg, respectively. Furthermore, we obtained an upward concave curvilinear pressure-volume area (PVA; a measure of total mechanical energy)-V (preload) relationship to assess LV work capability in each contractility. This relationship also shifted upward in enhanced contractility and downward in depressed contractility; the PVA at midrange V increased from 7.9 +/- 1.2 to 12.3 +/- 1.5 mmHg. ml.beat-1.g-1 and decreased from 8.2 +/- 0.9 to 6.4 +/- 0.8 mmHg.ml.beat-1.g-1. We conclude that the heights of the ESPVR and PVA-V relationship curves can evaluate LV contractility mechanoenergetically.


1988 ◽  
Vol 254 (2) ◽  
pp. H292-H303 ◽  
Author(s):  
H. Suga ◽  
Y. Goto ◽  
Y. Yasumura ◽  
T. Nozawa ◽  
S. Futaki ◽  
...  

We compared the effects of decreased coronary perfusion pressure (CP) and propranolol on the relation between left ventricular O2 consumption (VO2) and systolic pressure-volume area (PVA). PVA represents total mechanical energy generated by contraction and is the area under the end-systolic pressure-volume (PV) line and systolic PV trajectory. In excised cross-circulated dog hearts, a decrease in CP from 82 (mean) to 51 mmHg decreased ventricular contractility index Emax (slope of end-systolic PV relation) by 17% (P less than 0.05) and slightly (P less than 0.05 in 3 of 11 hearts) lowered the VO2-PVA relation in a parallel fashion. A further decrease in CP to 32 mmHg decreased Emax by 56% (P less than 0.05) and considerably (P less than 0.05) lowered the VO2-PVA relation by decreasing both the VO2-axis intercept by 26% (P less than 0.05) and the slope by 24% (P less than 0.05) from control. Propranolol decreased Emax by 48% (P less than 0.05) and the VO2-axis intercept by 25% (P less than 0.05) without changing the slope (P greater than 0.05). We attributed the different response of the VO2-PVA relation to the difference of the coronary O2 supply-demand balance between decreased CP and propranolol.


1992 ◽  
Vol 262 (3) ◽  
pp. H719-H727 ◽  
Author(s):  
Y. Goto ◽  
B. K. Slinker ◽  
M. M. LeWinter

To compare the effects of amrinone (AMR) and isoproterenol (Iso) on left ventricular contractility and energetics, we assessed Emax (ventricular contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA, a measure of left ventricular total mechanical energy) in isolated cross-circulated (blood-perfused) rabbit hearts during infusion of AMR or Iso in either a constant-flow (CF) or constant-pressure (CP) perfusion mode. Both Emax and the VO2 intercept of the linear VO2-PVA relation increased significantly during AMRCP (increase in Emax 15% and increase in VO2 intercept 11%), ISOCF (49 and 43%), and ISOCP (55 and 54%) but not during AMRCF. However, neither drug changed the slope of the VO2-PVA relation (reciprocal of contractile efficiency) in either perfusion mode. Furthermore, with both drugs the relation between increases in Emax and the VO2 intercept fell on a single regression line (r = 0.92). We conclude that 1) although the mechanism of action and inotropic potency of the two drugs differ, their effects on cardiac energetic cost are essentially the same, i.e., both drugs increase the nonmechanical oxygen cost in proportion to the increase in contractility without changing contractile efficiency, and 2) a significant portion of the inotropic effect of AMR in the whole ventricle is likely due to increased coronary blood flow, i.e., Gregg's phenomenon.


2019 ◽  
Vol 46 (5) ◽  
pp. 2137-2144
Author(s):  
Sahmin Lee ◽  
Seunghyun Choi ◽  
Sehwan Kim ◽  
Yeongjin Jeong ◽  
Kyusup Lee ◽  
...  

2021 ◽  
Author(s):  
Bálint Károly Lakatos ◽  
Mihály Ruppert ◽  
Márton Tokodi ◽  
Attila Oláh ◽  
Szilveszter Braun ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jorge Enrique Tovar Perez ◽  
Jesus Ortiz-Urbina ◽  
Celia Pena Heredia ◽  
Thuy T. Pham ◽  
Sridhar Madala ◽  
...  

An amendment to this paper has been published and can be accessed via a link at the top of the paper.


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