scholarly journals Effect of arterial impedance changes on the end-systolic pressure-volume relation.

1984 ◽  
Vol 54 (5) ◽  
pp. 595-602 ◽  
Author(s):  
W L Maughan ◽  
K Sunagawa ◽  
D Burkhoff ◽  
K Sagawa
Keyword(s):  
Systolic Pressure ◽  
Arterial Impedance ◽  
Volume Relation

Linear O2 Use-Pressure-Volume Area Relation from Curved End-Systolic Pressure-Volume Relation of the Blood-Perfused Rat Left Ventricle.

1998 ◽  
Vol 48 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Yoshiki HATA ◽  
Taisuke SAKAMOTO ◽  
Shingo HOSOGI ◽  
Tohru OHE ◽  
Hiroyuki SUGA ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Volume Relation

scholarly journals Linearity of the left ventricular end-systolic pressure-volume relation in patients with severe heart failure

1989 ◽  
Vol 14 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Constantine N. Aroney ◽  
Howard C. Herrmann ◽  
Marc J. Semigran ◽  
G. William ◽  
Charles A. Boucher ◽  
...  
Keyword(s):  
Heart Failure ◽  
Severe Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Relation

Similar normalized Emax and O2 consumption-pressure-volume area relation in rabbit and dog

1988 ◽  
Vol 255 (2) ◽  
pp. H366-H374 ◽  
Author(s):  
Y. Goto ◽  
B. K. Slinker ◽  
M. M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Energy Transduction ◽  
Base Line ◽  
Contractile State ◽  
Primary Determinant ◽  
Heart Size ◽  
Volume Relation

The end-systolic pressure-volume relation (ESPVR), a measure of ventricular contractile state, and systolic pressure-volume area (PVA), a primary determinant of cardiac oxygen consumption per beat (VO2), have been derived from the pressure-volume diagram of the cross-circulated dog left ventricle. The slope of the PVA-VO2 relation represents the efficiency of chemomechanical energy transduction of the contractile machinery. To see whether these relationships were similar in other animals, we studied the isovolumic ESPVR and the VO2-PVA relation in nine excised, cross-circulated rabbit left ventricles. The base-line ESPVR was linear (r = 0.94-0.99) with the slope (Emax) and volume-axis intercept (V0) equal to 83.4 +/- 18.3 mmHg/ml and 0.43 +/- 0.17 ml, respectively. When normalized for left ventricular weight, Emax (4.1 +/- 1.1 mmHg.ml-1.100 g) and V0 (8.9 +/- 3.7 ml/100 g) were similar to values reported for the dog left ventricle. The correlation between PVA and VO2 was linear (r = 0.93-1.00), and the slope (1.90 X 10(-5) +/- 0.44 X 10(-5) ml O2.mmHg-1.ml-1) and VO2-axis intercept (0.040 +/- 0.009 ml O2.beat-1.100 g-1) were similar to values found in the dog left ventricle. Hence, despite the greatly different heart size, the base-line contractile state and chemomechanical energy conversion efficiency of the excised, cross-circulated rabbit left ventricle are similar to those of the dog left ventricle.

Afterload Sensitivity of Nonlinear End-Systolic Pressure–Volume Relation vs Preload Recruitable Stroke Work in Conscious Dogs

1998 ◽  
Vol 75 (1) ◽  
pp. 6-17 ◽  
Author(s):  
L.Carr McClain ◽  
Leon D. Wright ◽  
Raj K. Bose ◽  
John A. Spratt ◽  
George W. Maier
Keyword(s):  
Systolic Pressure ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Volume Relation

scholarly journals Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction

2007 ◽  
Vol 292 (4) ◽  
pp. H1847-H1860 ◽  
Author(s):  
Marina R. Bergman ◽  
John R. Teerlink ◽  
Rajeev Mahimkar ◽  
Luyi Li ◽  
Bo-Qing Zhu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Matrix Metalloproteinase ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Membrane Type ◽  
Volume Relation

Although enhanced cardiac matrix metalloproteinase (MMP)-2 synthesis has been associated with ventricular remodeling and failure, whether MMP-2 expression is a direct mediator of this process is unknown. We generated transgenic mice expressing active MMP-2 driven by the α-myosin heavy chain promoter. At 4 mo MMP-2 transgenic hearts demonstrated expression of the MMP-2 transgene, myocyte hypertrophy, breakdown of Z-band registration, lysis of myofilaments, disruption of sarcomere and mitochondrial architecture, and cardiac fibroblast proliferation. Hearts from 8-mo-old transgenic mice displayed extensive myocyte disorganization and dropout with replacement fibrosis and perivascular fibrosis. Older transgenic mice also exhibited a massive increase in cardiac MMP-2 expression, representing recruitment of endogenous MMP-2 synthesis, with associated expression of MMP-9 and membrane type 1 MMP. Increases in diastolic [control (C) 33 ± 3 vs. MMP 51 ± 12 μl; P = 0.003] and systolic (C 7 ± 2 vs. MMP 28 ± 14 μl; P = 0.003) left ventricular (LV) volumes and relatively preserved stroke volume (C 26 ± 4 vs. MMP 23 ± 3 μl; P = 0.16) resulted in markedly decreased LV ejection fraction (C 78 ± 7% vs. MMP 48 ± 16%; P = 0.0006). Markedly impaired systolic function in the MMP transgenic mice was demonstrated in the reduced preload-adjusted maximal power (C 240 ± 84 vs. MMP 78 ± 49 mW/μl2; P = 0.0003) and decreased end-systolic pressure-volume relation (C 7.5 ± 1.5 vs. MMP 4.7 ± 2.0; P = 0.016). Expression of active MMP-2 is sufficient to induce severe ventricular remodeling and systolic dysfunction in the absence of superimposed injury.

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