Stability of myocardial O2 consumption-pressure-volume area relation in red cell-perfused rabbit heart

1991 ◽  
Vol 261 (5) ◽  
pp. H1630-H1635
Author(s):  
H. Yaku ◽  
B. K. Slinker ◽  
E. S. Myhre ◽  
M. W. Watkins ◽  
M. M. Lewinter
Keyword(s):  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Rabbit Heart ◽  
Cardiac Contraction ◽  
Red Cell ◽  
O2 Consumption ◽  
Perfused Rabbit Heart ◽  
Total Mechanical Energy ◽  
Heart Preparation ◽  
Myocardial O2 Consumption

We evaluated the mechanical and energetic stability of the isolated rabbit heart perfused with a suspension of bovine red cells in Krebs-Henseleit buffer in terms of the pressure-volume area (PVA) concept. PVA, the area surrounded by the end-systolic and end-diastolic pressure-volume (P-V) relations and the systolic P-V trajectory of the P-V diagram, represents the total mechanical energy generated by each cardiac contraction. Myocardial O2 consumption (VO2) per beat has been reported to be highly linearly correlated with PVA. We used the slope and VO2-axis intercept of the VO2-PVA relation as energetic parameters and the maximum P-V ratio (Emax) as a contractility index of the left ventricle (LV) and compared them every 30 min for 120 min. Emax, the slope, and VO2 intercept of the VO2-PVA relation did not change significantly over 120 min compared with their control values [7.3 +/- 2.9 mmHg.ml-1.100 g LV, (1.67 +/- 0.40) x 10(-5) ml O2.mmHg-1.ml-1, and (3.26 +/- 1.01) x 10(-2) ml O2.beat-1.100 g LV-1, respectively]. However, the goodness of the linear fit of the VO2-PVA relation decreased after 90 min (r = 0.94 control, 0.62 at 90 min, and 0.64 at 120 min). Therefore, we conclude that the isolated bovine red cell-perfused rabbit heart preparation is stable for mechanical and energetic studies for at least 60 min.

Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics

2009 ◽  
Vol 297 (5) ◽  
pp. H1736-H1743 ◽  
Author(s):  
Chikako Nakajima-Takenaka ◽  
Guo-Xing Zhang ◽  
Koji Obata ◽  
Kiyoe Tohne ◽  
Hiroko Matsuyoshi ◽  
...  
Keyword(s):  
Relaxation Rate ◽  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Mechanical Work ◽  
Linear Relations ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Heart Preparation

We investigated left ventricular (LV) mechanical work and energetics in the cross-circulated (blood-perfused) isoproterenol [Iso 1.2 mg·kg−1·day−1 for 3 days (Iso3) or 7 days (Iso7)]-induced hypertrophied rat heart preparation under isovolumic contraction-relaxation. We evaluated pressure-time curves per beat, end-systolic pressure-volume and end-diastolic pressure-volume relations, and myocardial O2 consumption per beat (V̇o2)-systolic pressure-volume area (PVA; a total mechanical energy per beat) linear relations at 240 beats/min, because Iso-induced hypertrophied hearts failed to completely relax at 300 beats/min. The LV relaxation rate at 240 beats/min in Iso-induced hypertrophied hearts was significantly slower than that in control hearts [saline 24 μl/day for 3 and 7 days (Sa)] with unchanged contraction rate. The V̇o2-intercepts (composed of basal metabolism and Ca2+ cycling energy consumption in excitation-contraction coupling) of V̇o2-PVA linear relations were unchanged associated with their unchanged slopes in Sa, Iso3, and Iso7 groups. The oxygen costs of LV contractility were also unchanged in all three groups. The amounts of expression of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), phosphorylated-Ser16 PLB, phospholemman, and Na+-K+-ATPase are significantly decreased in Iso3 and Iso7 groups, although the amount of expression of NCX1 is unchanged in all three groups. Furthermore, the marked collagen production (types I and III) was observed in Iso3 and Iso7 groups. These results suggested the possibility that lowering the heart rate was beneficial to improve mechanical work and energetics in isoproterenol-induced hypertrophied rat hearts, although LV relaxation rate was slower than in normal hearts.

Prospective prediction of O2 consumption from pressure-volume area in dog hearts

1987 ◽  
Vol 252 (6) ◽  
pp. H1258-H1264 ◽  
Author(s):  
H. Suga ◽  
Y. Yasumura ◽  
T. Nozawa ◽  
S. Futaki ◽  
Y. Igarashi ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Regression Coefficients ◽  
Coefficient Of Determination ◽  
O2 Consumption ◽  
Ventricular Contraction ◽  
Individual Variations ◽  
Total Mechanical Energy ◽  
Myocardial O2 Consumption ◽  
The Individual

Systolic pressure-volume area (PVA) is the area circumscribed by the end-systolic pressure-volume (PV) line, the end-diastolic PV curve, and the systolic PV trajectory of the ventricle. PVA represents the total mechanical energy generated by ventricular contraction. Myocardial O2 consumption (VO2) linearly correlates with PVA under different pre- and afterloads in the dog left ventricle. The linear VO2-PVA relation parallel shifts with changes in contractility index Emax. We have retrospectively obtained VO2 = A X PVA + B . Emax + C, where A, B, and C are regression coefficients. We used this equation to prospectively predict VO2 from measured PVA and Emax in a new group of dog left ventricles. Coefficient of determination (CD) of measured VO2 from predicted VO2 was 0.86 +/- 0.09 (SD) in individual hearts, but decreased to 0.72 when data of the five hearts were pooled. These prospective CDs in individual hearts and all hearts were smaller than retrospective CDs in the individual hearts (0.90 +/- 0.06). Inter-individual variations of A,B, and C caused the lower prospective predictability.

Equivalent pressure-volume area accounts for oxygen consumption of fibrillating heart

1991 ◽  
Vol 261 (5) ◽  
pp. H1534-H1544
Author(s):  
H. Yaku ◽  
Y. Goto ◽  
S. Futaki ◽  
Y. Ohgoshi ◽  
O. Kawaguchi ◽  
...  
Keyword(s):  
Regression Coefficient ◽  
Mechanical Energy ◽  
Regression Line ◽  
Ventricular Volume ◽  
Canine Heart ◽  
Ventricular Volumes ◽  
Identity Line ◽  
Total Mechanical Energy ◽  
Heart Preparation ◽  
Myocardial O2 Consumption

We attempted to find cardiac mechanical parameters to account for myocardial O2 consumption (VO2) during ventricular fibrillation (VF). We fully utilized the concept of pressure-volume (P-V) area (PVA), which is equivalent to the total mechanical energy generated by a ventricular contraction. We also utilized a multicompartment model consisting of multiple asynchronously contracting compartments, which we previously proposed to simulate the mechanics of a fibrillating ventricle. The model analysis had already validated the application of PVA to VF in terms of "equivalent PVA" (ePVA). ePVA is the area surrounded by the end-systolic and end-diastolic P-V relations in beating state and the isobaric P-V line at the VF pressure. ePVA is supposed to represent the total mechanical energy generated by single contractions of each compartment (or myocyte) in a fibrillating ventricle. We determined ePVA and correlated it with measured VO2 per minute (mVO2) at various ventricular volumes in electrically induced fibrillating left ventricles of the excised cross-circulated canine heart preparation. Correlation coefficient (r) of the mVO2-ePVA relation during VF was high (r = 0.95, P less than 0.01). Comparing mVO2 during VF with that in beating state at an unloaded ventricular volume, we calculated equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual compartments (myocytes). With the use of both ePVA and eHR, mVO2 during VF at various ventricular volumes was estimated. The relation between estimated mVO2 and directly measured mVO2 was highly linear (r = 0.88, P less than 0.01), and the regression line almost agreed with the identity line (regression coefficient = 1.05). We conclude that the new ePVA and eHR concepts can reasonably account for VO2 during VF.

Mechanoenergetics of negative inotropism of ventricular wall vibration in dog heart

1996 ◽  
Vol 270 (2) ◽  
pp. H583-H593 ◽  
Author(s):  
T. Nishioka ◽  
Y. Goto ◽  
K. Hata ◽  
T. Takasago ◽  
A. Saeki ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Mechanical Vibration ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Cardiac Contraction ◽  
Wall Region ◽  
Dog Heart ◽  
Negative Inotropism ◽  
Total Mechanical Energy ◽  
Heart Preparation

Mechanical vibration depresses cardiac contractility. We studied the mechanoenergetic effects of this negative inotropism in the left ventricle (LV) of an isolated, cross-circulated dog heart preparation. We took full advantage of the mechanoenergetic relationship among the LV end-systolic elastance (Emax, contractility index), systolic pressure-volume area (PVA), and myocardial oxygen consumption (VO2). PVA is a measure of the total mechanical energy that cardiac contraction generates. PVA correlates closely with VO2. The VO2 intercept of the VO2-PVA relation reflects the VO2 component for excitation-contraction (E-C) coupling plus basal metabolism (PVA-independent VO2). VO2 above the PVA-independent VO2 reflects the VO2 component for mechanical contraction (PVA-dependent VO2). When we applied 70-Hz vibration of 2-mm amplitude to a LV wall region, it instantly decreased Emax and PVA by 20%, followed by a 10% decrease in VO2 at a fixed volume. However, the vibration neither lowered the VO2-PVA relation obtained at different LV volumes, unlike ordinary negative inotropism, nor changed its slope (1.88 +/- 0.23 vs. 1.86 +/- 0.23 x 10(-5) ml O2.mmHg-1.ml-1). The virtually zero delta PVA-independent VO2/delta Emax with vibration indicates a much smaller O2 cost of Emax than that seen with calcium and propranolol inotropism. These mechanoenergetics support the hypothesis that mechanical vibration primarily suppresses cardiac contractility without suppressing E-C coupling.

Preload does not influence nonmechanical O2 consumption in isolated rabbit heart

1994 ◽  
Vol 266 (3) ◽  
pp. H1047-H1054 ◽  
Author(s):  
A. Higashiyama ◽  
M. W. Watkins ◽  
Z. Chen ◽  
M. M. LeWinter
Keyword(s):  
Energy Consumption ◽  
Diastolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Energetic Cost ◽  
O2 Consumption ◽  
Time Integral ◽  
Force Time ◽  
Whole Heart ◽  
Force Time Integral

Myocardial energy consumption for nonmechanical activity (excitation-contraction coupling) has been shown to be length dependent in isolated muscle studies but no more than minimally affected by preload in the whole heart. However, unloaded O2 consumption (VO2, which is used to estimate nonmechanical VO2 in whole heart) may not be accurate for quantifying nonmechanical energy consumption, because it contains VO2 for residual cross-bridge cycling. To more accurately determine the influence of left ventricular (LV) diastolic volume on nonmechanical VO2 in whole heart, we employed a new method for quantifying nonmechanical VO2, using the drug 2,3-butanedione monoxime (BDM). We measured VO2 and force-time integral during infusion of BDM (< or = 5 mM) at high (VH) and low LV volumes (VL) in 16 excised isovolumically contracting red blood cell-perfused rabbit ventricles. LV end-diastolic pressure was 9.7 +/- 4.6 and 3.8 +/- 2.8 (SD) mmHg at VH and VL, respectively. Nonmechanical VO2, estimated as the VO2-axis intercept of the linear VO2-force-time integral relation obtained during BDM infusion, did not differ significantly between VH and VL (0.0137 +/- 0.0083 and 0.0132 +/- 0.0090 ml O2.beat-1 x 100 gLV-1, P = 0.702). A multiple linear regression analysis for the pooled data confirmed this finding (P = 0.361). We conclude that, in the rabbit heart, LV diastolic volume does not importantly affect nonmechanical energy consumption over a physiological range of LV end-diastolic pressure. This indicates that length-dependent activation does not have an energetic cost in whole rabbit heart and suggests that its predominant mechanism is increased Ca2+ affinity for the contractile proteins.

Consistent substrate utilization despite reduced flow in hearts with maintained work

1983 ◽  
Vol 244 (6) ◽  
pp. H799-H806 ◽  
Author(s):  
K. A. Fox ◽  
H. Nomura ◽  
B. E. Sobel ◽  
S. R. Bergmann
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Myocardial Metabolism ◽  
Diastolic Pressure ◽  
Rabbit Heart ◽  
Substrate Utilization ◽  
Left Ventricular ◽  
Low Flow ◽  
Heart Preparation

Assessments of myocardial metabolism based on external detection of accumulation of radiolabeled substrates may be influenced, as a result of alterations in flow, by altered substrate delivery as well as altered work (with concomitant changes in metabolic requirements). To determine whether reduced delivery limits substrate utilization under defined conditions of reduced perfusion, an isolated rabbit heart preparation was employed in which flow was reduced but myocardial oxygen consumption (MVo2) and work were kept constant by adjustment of left ventricular end-diastolic pressure and heart rate. Flow was reduced from 1.5 to 0.5 ml . g-1 . min-1, while work was maintained constant in hearts functioning at either low or high levels of MVo2. Consumption of palmitate remained constant (48.8 +/- 11.6 and 68.8 +/- 23.3 nmol . g-1 . min-1), because the proportion of palmitate extracted increased (8.8 +/- 4 to 29.1 +/- 7.2% and 10.3 +/- 3.4 to 21.0 +/- 6.1%). The results indicate that, despite reduction of flow, hearts at constant work loads can extract increasing proportions of delivered substrates such that net utilization remains constant until flow is reduced below the level required to maintain cellular function. They suggest that, under conditions of low flow, impaired extraction of substrates reflects either primarily or secondarily depressed myocardial metabolism rather than simply decreased delivery of substrate.

Sensitivities of cardiac O2 consumption and contractility to catecholamines in dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H196-H205 ◽  
Author(s):  
Y. Ohgoshi ◽  
Y. Goto ◽  
S. Futaki ◽  
H. Yaku ◽  
H. Suga
Keyword(s):  
Mechanical Energy ◽  
Plasma Catecholamines ◽  
Systolic Pressure ◽  
Plasma Catecholamine ◽  
Catecholamine Level ◽  
Oxygen Cost ◽  
O2 Consumption ◽  
Total Mechanical Energy ◽  
Plasma Catecholamine Level ◽  
Stimulation Of

We studied the effects of plasma catecholamines from the adrenal gland on systolic pressure-volume area (PVA)-independent O2 consumption (VO2) and contractility index (Emax) in the left ventricle of excised cross-circulated dog hearts. PVA is a measure of the total mechanical energy of contraction. Under baseline conditions, the PVA-independent VO2 correlated with plasma catecholamine level in the hearts (r = 0.84). Plasma epinephrine and norepinephrine levels increased gradually from 0.3 and 0.4 ng/ml to 10.3 and 2.7 ng/ml on average during adrenal sympathetic nerve stimulation of support dogs. Simultaneously, Emax and PVA-independent VO2 increased by 240 +/- 127 (SD) and 75 +/- 24%. Although their increases were monotonic in a given heart, their sensitivities to catecholamines were considerably variable among hearts. However, these two sensitivities were correlated (r = 0.96) with each other in the hearts, and the interheart variation of the sensitivity of the PVA-independent VO2 to Emax (i.e., oxygen cost of Emax) was smaller. We conclude that the oxygen cost of Emax is less variable among hearts despite large interheart variations of Emax and VO2 responses to plasma catecholamines.

Independent role of arterial O2 tension in local control of coronary blood flow

1990 ◽  
Vol 258 (5) ◽  
pp. H1388-H1394 ◽  
Author(s):  
J. F. Baron ◽  
E. Vicaut ◽  
X. Hou ◽  
M. Duvelleroy
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Perfusion Pressure ◽  
Rabbit Heart ◽  
Coronary Resistance ◽  
Heart Preparation ◽  
Myocardial O2 Consumption ◽  
O2 Delivery ◽  
Arterial Po2

The aim of this study of a blood-perfused isolated rabbit heart preparation was to differentiate the effects on coronary resistance of large changes in arterial O2 tension (arterial PO2 = 45-400 Torr) from the effects of variations in arterial O2 content or myocardial O2 delivery. Standard stored human blood was resuspended in Krebs-Henseleit buffer and was oxygenated to obtain normal PO2, high PO2, and low PO2. Hemoglobin concentrations were adjusted to obtain the same arterial O2 content (CaO2) for the three PO2s. In a first set of experiments, in which coronary blood flow (CBF) was free and adapted to a constant perfusion pressure, switching from control [138 +/- 17 (SE) Torr] to high PO2 blood (380 +/- 27 Torr) induced a significant decrease in CBF and myocardial O2 consumption (MVO2). Switching from control (125 +/- 3 Torr) to low PO2 blood (49 +/- 5 Torr) induced a significant increase in CBF and MVO2. In a second set of experiments, the switch from control (159 +/- 5 Torr) to high PO2 (389 +/- 32 Torr) was performed in a preparation in which CBF and consequently O2 delivery were constant. Under these conditions, the increase in perfusion pressure demonstrated that PO2 affected coronary resistance, even though the O2 delivery was constant. No significant change in myocardial performance was observed in any of these experimental procedures. These results show that arterial PO2 may affect coronary blood flow regulation independently of any mediation by the autonomic nervous system and of any associated changes in O2 content or O2 delivery.

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