New mechanoenergetic evaluation of left ventricular contractility in in situ rat hearts

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.

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

The Japanese Journal of Physiology ◽

10.2170/jjphysiol.rp000405 ◽

2005 ◽

Vol 55 (5) ◽

pp. 255-264 ◽

Cited By ~ 2

Author(s):

Satoshi Mohri ◽

Juichiro Shimizu ◽

Haruo Ito ◽

Hiroki Yamaguchi ◽

Shunji Sano ◽

...

Keyword(s):

Atrial Fibrillation ◽

Mechanical Energy ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Normal Distributions ◽

Unstressed Volume ◽

Total Mechanical Energy

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00672.2009 ◽

2009 ◽

Vol 297 (5) ◽

pp. H1736-H1743 ◽

Cited By ~ 10

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.

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Assessment of slope of end-systolic pressure-volume line of in situ dog heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.250.4.h685 ◽

1986 ◽

Vol 250 (4) ◽

pp. H685-H692 ◽

Cited By ~ 1

Author(s):

Y. Igarashi ◽

H. Suga

Keyword(s):

Systolic Pressure ◽

Electromagnetic Flowmeter ◽

Left Ventricular ◽

Aortic Occlusion ◽

Atrial Pacing ◽

Ventricular Contractility ◽

Dog Heart ◽

End Diastolic Volume ◽

Isovolumic Contraction

The purpose of this study was to establish a new method of assessment of the slope (Emax) of the end-systolic pressure-volume line (ESPVL) of the in situ heart. In anesthetized open-chest dogs, an isovolumic contraction was produced by an aortic occlusion after steady-state ejecting contractions in the left ventricle. We plotted ventricular pressure measured with a catheter-tip manometer against time integral of aortic flow measured with an electromagnetic flowmeter of the last ejecting and the first isovolumic contraction, assuming the same end-diastolic volume. ESPVL was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the +/- 3.0 (SE) mmHg/ml (n = 9 dogs) in control run and was increased by 59 +/- 19% under isoproterenol and decreased by 47 +/- 9% after propranolol. Emax was little changed by atrial pacing. We conclude that Emax by this aortic occlusion method is useful for assessment of left ventricular contractility of the in situ dog heart.

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Oxygen Costs of Left Ventricular Contractility for Dobutamine and Ca2+ in Normal Rat Hearts and the Cost for Dobutamine in Ca2+ Overload-Induced Failing Hearts.

The Japanese Journal of Physiology ◽

10.2170/jjphysiol.52.163 ◽

2002 ◽

Vol 52 (2) ◽

pp. 163-171 ◽

Cited By ~ 11

Author(s):

Nobuoki Tabayashi ◽

Takehisa Abe ◽

Shuichi Kobayashi ◽

Yoshiro Yoshikawa ◽

Susumu Sakata ◽

...

Keyword(s):

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Rat Hearts ◽

Normal Rat ◽

The Cost

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Reversible effects of isoproterenol-induced hypertrophy on in situ left ventricular function in rat hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00073.2004 ◽

2004 ◽

Vol 287 (1) ◽

pp. H277-H285 ◽

Cited By ~ 23

Author(s):

Yutaka Kitagawa ◽

Daisuke Yamashita ◽

Haruo Ito ◽

Miyako Takaki

Keyword(s):

Cardiac Hypertrophy ◽

Systolic Pressure ◽

Left Ventricular ◽

Lv Function ◽

Osmotic Minipump ◽

Good Index ◽

Rat Hearts ◽

Lv Volume ◽

Work Capability

The aim of the present study was to evaluate specifically left ventricular (LV) function in rat hearts as they transition from the normal to hypertrophic state and back to normal. Either isoproterenol (1.2 and 2.4 mg·kg−1·day−1 for 3 days; Iso group) or vehicle (saline 24 μl·day−1 for 3 days; Sa group) was infused by subcutaneous implantation of an osmotic minipump. After verifying the development of cardiac hypertrophy, we recorded continuous LV pressure-volume (P-V) loops of in situ ejecting hypertrophied rat hearts. The curved LV end-systolic P-V relation (ESPVR) and systolic P-V area (PVA) were obtained from a series of LV P-V loops in the Sa and Iso groups 1 h or 2 days after the removal of the osmotic minipump. PVA at midrange LV volume (PVAmLVV) was taken as a good index for LV work capability ( 13 , 15 , 20 , 21 ). However, in rat hearts during remodeling, whether PVAmLVV is a good index for LV work capability has not been determined yet. In the present study, in contrast to unchanged end-systolic pressure at midrange LV volume, PVAmLVV was significantly decreased by isoproterenol treatment relative to saline; however, these measurements were the same 2 days after pump removal. Simultaneous treatment with a β1-blocker, metoprolol (24 mg·kg−1·day−1), blocked the formation of cardiac hypertrophy and thus PVAmLVV did not decrease. The reversible changes in PVAmLVV reflect precisely the changes in LV work capability in isoproterenol-induced hypertrophied rat hearts mediated by β1-receptors. These results indicate that the present approach may be an appropriate strategy for evaluating the effects of antihypertrophic and antifibrotic modalities.

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Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01033.2004 ◽

2005 ◽

Vol 288 (4) ◽

pp. H1699-H1707 ◽

Cited By ~ 27

Author(s):

Hiroji Hagihara ◽

Yoshiro Yoshikawa ◽

Yoshimi Ohga ◽

Chikako Takenaka ◽

Ken-ya Murata ◽

...

Keyword(s):

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Mechanical Energy ◽

Ischemia Reperfusion ◽

Systolic Pressure ◽

Left Ventricular ◽

Reverse Mode ◽

Rat Hearts ◽

Total Mechanical Energy ◽

Contractile Failure

We have recently reported that exposure of rat hearts to high Ca2+ produces a Ca2+ overload-induced contractile failure in rat hearts, which was associated with proteolysis of α-fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVAmLVV) was significantly decreased from 5.89 ± 1.55 to 3.83 ± 1.16 mmHg·ml·beat−1·g−1 ( n = 6). Mean myocardial oxygen consumption per beat (Vo2) intercept of (Vo2-PVA linear relation was significantly decreased from 0.21 ± 0.05 to 0.15 ± 0.03 μl O2·beat−1·g−1 without change in its slope. Initial 30-min reperfusion with a Na+/Ca2+ exchanger (NCX) inhibitor KB-R7943 (KBR; 10 μmol/l) significantly reduced the decrease in mean PVAmLVV and Vo2 intercept ( n = 6). Although Vo2 for the Ca2+ handling was finally decreased, it transiently but significantly increased from the control for 10–15 min after I/R. This increase in Vo2 for the Ca2+ handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. α-Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca2+ infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.

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O2 consumption of dog heart under decreased coronary perfusion and propranolol

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.2.h292 ◽

1988 ◽

Vol 254 (2) ◽

pp. H292-H303 ◽

Cited By ~ 3

Author(s):

H. Suga ◽

Y. Goto ◽

Y. Yasumura ◽

T. Nozawa ◽

S. Futaki ◽

...

Keyword(s):

Mechanical Energy ◽

Systolic Pressure ◽

Coronary Perfusion Pressure ◽

Left Ventricular ◽

Coronary Perfusion ◽

O2 Consumption ◽

Ventricular Contractility ◽

Total Mechanical Energy ◽

The Difference ◽

Different Response

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.

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Effects of amrinone and isoproterenol on mechanoenergetics of blood-perfused rabbit heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.3.h719 ◽

1992 ◽

Vol 262 (3) ◽

pp. H719-H727 ◽

Cited By ~ 2

Author(s):

Y. Goto ◽

B. K. Slinker ◽

M. M. LeWinter

Keyword(s):

Mechanical Energy ◽

Regression Line ◽

Systolic Pressure ◽

Rabbit Heart ◽

Left Ventricular ◽

Energetic Cost ◽

Ventricular Contractility ◽

Total Mechanical Energy ◽

Single Regression ◽

Perfusion Mode

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.

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