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.

Transient vs. steady end-systolic pressure-volume relation in dog left ventricle

1987 ◽  
Vol 252 (5) ◽  
pp. H998-H1004 ◽  
Author(s):  
Y. Igarashi ◽  
Y. Goto ◽  
O. Yamada ◽  
T. Ishii ◽  
H. Suga
Keyword(s):  
Regression Analysis ◽  
Steady State ◽  
Linear Regression ◽  
Left Ventricle ◽  
Ejection Fraction ◽  
Linear Regression Analysis ◽  
Systolic Pressure ◽  
Contractile State ◽  
End Diastolic Volume ◽  
Volume Relation

We compared transient slope of end-systolic pressure-volume line (T-Emax) with steady Emax (S-Emax) in isolated cross-circulated canine left ventricles. T-Emax is the slope of the end-systolic pressure-volume line (ESPVL) determined from the last steady-state ejecting contraction (SEC) and the first transient isovolumic contraction produced by end-diastolic volume clamp. S-Emax is the slope of ESPVL determined from five steady-state contractions by linear regression analysis. We obtained three T-Emax values in the same contractile state by changing ejection fraction (EF) of SEC to three levels (range 14-58%) from the same end-diastolic volume. T-Emax variably increased with EF in any contractile state. The ratios of the three T-Emax values to the same S-Emax value was 1.08 +/- 0.04 (11 ventricles, means +/- SE) for high EF, 0.87 +/- 0.06 for middle EF, and 0.69 +/- 0.07 for low EF in control contractile state. These ratios decreased under epinephrine and increased under propranolol. We conclude that T-Emax depends not only on EF but also on contractile state in isolated dog left ventricles.

Left ventricular O2 consumption and pressure-volume area in puppies

1987 ◽  
Vol 253 (4) ◽  
pp. H770-H776 ◽  
Author(s):  
H. Suga ◽  
O. Yamada ◽  
Y. Goto ◽  
Y. Igarashi ◽  
Y. Yasumura ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Regression Line ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
O2 Consumption ◽  
Ventricular Contraction ◽  
Myocardial Mechanics ◽  
Contractile State ◽  
Total Mechanical Energy ◽  
Heart Size

We studied the relation between O2 consumption (VO2) and systolic pressure-volume (PV) area (PVA) in the left ventricles of eight puppies (2-4 mo old). PVA is the area circumscribed by the end-systolic and end-diastolic PV curves and systolic PV trajectory. We assumed PVA to represent the total mechanical energy generated by ventricular contraction. We produced isovolumic contractions at different volumes in the left ventricles isolated and cross-circulated with adult dogs. VO2 closely correlated with PVA in each of control contractile state, an enhanced contractile state with epinephrine, and a depressed contractile state with propranolol in each heart. The slope of the regression line of VO2 on PVA was not significantly affected by epinephrine and propranolol. The regression line shifted upward with epinephrine and downward with propranolol. These characteristics of the puppy's VO2-PVA relation were comparable to those of the adult dog. These results suggest that similar relations hold between myocardial mechanics and energetics in both the puppy and adult dog despite the differences in the heart size and contractile properties.

Effect of dobutamine of ventriculoarterial coupling in acute regional myocardial ischemia in dogs

1996 ◽  
Vol 270 (4) ◽  
pp. H1279-H1286
Author(s):  
H. Seki ◽  
K. Katayama ◽  
H. Sakai ◽  
T. Yonezawa ◽  
H. Kunichika ◽  
...  
Keyword(s):  
Low Dose ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
High Dose ◽  
Base Line ◽  
Work Efficiency ◽  
External Work ◽  
Regional Ischemia ◽  
Volume Relation ◽  
Acute Regional Ischemia

We assessed the effect of dobutamine on left ventricoarterial coupling during acute regional ischemia. Using a conductance catheter, we analyzed the end-systolic pressure-volume relation (ESPVR) in anesthetized dogs. We calculated the slope of ESPVR (Ees), the slope of the end-systolic pressure-stroke volume relation (Ea), (Ea/Ees) and the ratio (work efficiency) of external work to pressure-volume area at base-line during ischemia induced by occlusion of the left anterior descending coronary artery and during low-dose (1-3 micrograms.min-1.kg-1) and high-dose (4-10 micrograms.min-1.kg-1)dobutamine infusions with ischemia. ESPVR shifted to the right without a change in Ees during ischemia. Dobutamine caused dose-dependent increases in Ees but did not affect the intercept of ESPVR. During ischemia, Ea/Ees increased and work efficiency decreased. Low-dose dobutamine was associated with a return in control for Ea/Ees and work efficiency. High-dose dobutamine increased Ees and Ea but produced no further increase in Ea/Ees or work efficiency. Low-dose dobutamine would appear to be the preferable regimen to achieve the optimal ventriculoarterial coupling in acute regional ischemia associated with mismatched ventriculoarterial coupling and depressed left ventricular work efficiency.

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

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Role of Diastole in Left Ventricular Function, I: Biochemical and Biomechanical Events

2004 ◽  
Vol 13 (5) ◽  
pp. 394-403 ◽  
Author(s):  
Penelope S. Villars ◽  
Shannan K. Hamlin ◽  
Andrew D. Shaw ◽  
Joseph T. Kanusky
Keyword(s):  
Left Ventricle ◽  
Calcium Release ◽  
Troponin I ◽  
Regulatory Protein ◽  
Systolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Release Mechanism ◽  
Adrenergic Stimulation ◽  
Inotropic State

Left ventricular diastolic function plays an important role in cardiac physiology. Lusitropy, the ability of the cardiac myocytes to relax, is affected by both biochemical events within the myocyte and biomechanical events in the left ventricle. β-Adrenergic stimulation alters diastole by enhancing the phosphorylation of phospholamban, a substrate within the myocyte that increases the uptake of calcium ions into the sarcoplasmic reticulum, increasing the rate of relaxation. Troponin I, a regulatory protein involved in the coupling of excitation to contraction, is vital to maintaining the diastolic state; depletion of troponin I can produce diastolic dysfunction. Other biochemical events, such as defects in the voltage-sensitive release mechanism or in inositol triphosphate calcium release channels, have also been implicated in altering diastolic tone. Extracellular collagen determines myocardial stiffness; impaired glucose tolerance can induce an increase in collagen cross-linking and lead to higher end-diastolic pressures. The passive properties of the left ventricle are most accurately measured during the diastasis and atrial contraction phases of diastole. These phases of the cardiac cycle are the least affected by volume status, afterload, inherent viscoelasticity, and the inotropic state of the myocardium. Diastolic abnormalities can be conceptualized by using pressure-volume loops that illustrate myocardial work and both diastolic and systolic pressure-volume relationships. The pressure-volume model is an educational tool that can be used to demonstrate isolated changes in preload, afterload, inotropy, and lusitropy and their interaction.

Left ventricular force-length relations of isovolumic and ejecting contractions

1976 ◽  
Vol 231 (2) ◽  
pp. 337-343 ◽  
Author(s):  
KT Weber ◽  
JS Janicki ◽  
LL Hefner
Keyword(s):  
Left Ventricle ◽  
Linear Function ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Sectional Area ◽  
Active Force ◽  
Cross Sectional ◽  
Contractile State ◽  
State Dependent ◽  
Ejection Pressure

To determine the interrelationships between ejecting and isovolumic force-length relations and the extent to which the left ventricle will shorten, data obtained in 27 isolated, servo-regulated hearts were examined. For each heart a series of contractions, variably loaded (delta L) were derived for a thickwalled sphere and normalized by the cross-sectional area of muscle and length at zero end-diastolic pressure. It was found that within the physiological range examined total and active force were essentially a linear function of initial L with respective increments or reductions in slope produced by positive or negative shifts in contractile state. The force-L relations obtained isovolumically and at end ejection were virtually identical. For a given ejection pressure, end-systolic L was constant, despite variations in filling and therefore independent of initial L and deltaL; moreover, the L to which the ventricle shortened was determined by the course of the systolic force L-relation. Thus, irrespective of loading, delta L occurs within the confines of the contractile state-dependent isovolumic force-L relation and where the latter is equivalent to the end-systolic force-length relation.

Severe diastolic dysfunction with preserved energy conversion efficiency after countershock

1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto
Keyword(s):  
Diastolic Dysfunction ◽  
Mechanical Performance ◽  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Myocardial Edema ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Before And After

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.

Sign in / Sign up

Export Citation Format

Share Document