Predictability of O2 Consumption from Contractility and Mechanical Energy of Absolute Arrhythmic Beats in Canine Heart

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.

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Sensitivities of cardiac O2 consumption and contractility to catecholamines in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.1.h196 ◽

1991 ◽

Vol 261 (1) ◽

pp. H196-H205 ◽

Cited By ~ 2

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.

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Heart rate-independent energetics and systolic pressure-volume area in dog heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.2.h206 ◽

1983 ◽

Vol 244 (2) ◽

pp. H206-H214 ◽

Cited By ~ 12

Author(s):

H. Suga ◽

R. Hisano ◽

S. Hirata ◽

T. Hayashi ◽

O. Yamada ◽

...

Keyword(s):

Heart Rate ◽

Oxygen Consumption ◽

Left Ventricle ◽

Mechanical Energy ◽

Systolic Pressure ◽

Left Ventricular ◽

Canine Heart ◽

Heart Rates ◽

Dog Heart ◽

Total Mechanical Energy

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.6.h1258 ◽

1987 ◽

Vol 252 (6) ◽

pp. H1258-H1264 ◽

Cited By ~ 6

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.

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Effects of Intracoronary Fentanyl on Left Ventricular Mechanoenergetics in the Excised Cross-circulated Canine Heart (Revised Publication)

Anesthesiology ◽

10.1097/00000542-199709000-00028 ◽

1997 ◽

Vol 87 (3) ◽

pp. 658-666 ◽

Cited By ~ 7

Author(s):

Kunihisa Kohno ◽

Miyako Takaki ◽

Kazunari Ishioka ◽

Yasunori Nakayama ◽

Shunsuke Suzuki ◽

...

Keyword(s):

Oxygen Consumption ◽

Energy Use ◽

Mechanical Energy ◽

Systolic Pressure ◽

Left Ventricular ◽

Canine Heart ◽

Loading Conditions ◽

Wide Range ◽

Total Mechanical Energy ◽

Lv Volumes

Background It is still unclear whether fentanyl directly alters left ventricular (LV) contractility and oxygen consumption. This is because of the difficulty in defining and evaluating contractility and energy use independently of ventricular loading conditions and heart rate in beating whole hearts. Methods This study was conducted to clarify the mechanoenergetic effects of intracoronary fentanyl in six excised cross-circulated canine hearts. The authors used the framework of the Emax (a contractility index)-PVA (systolic pressure-volume area, a measure of total mechanical energy)-VO2 (myocardial oxygen consumption per beat) relationship practically independent of ventricular loading conditions. The authors measured LV pressure, volume, coronary flow, and arteriovenous oxygen content difference to calculate Emax, PVA, and VO2. They first obtained the VO2-PVA relationship for varied LV volumes at control Emax. The authors then obtained the VO2-PVA relationship at a constant LV volume, whereas coronary blood fentanyl concentration was increased in steps up to 240 ng/ml. Finally, they obtained the VO2-PVA relationship for varied LV volumes at the final dose of fentanyl. Results Fentanyl at any concentrations did not significantly change Emax, PVA, and VO2 from the control. The linear end-systolic pressure-volume relations and their slopes were virtually the same between the control and fentanyl volume loading in each heart. Further, either the slope (oxygen cost of PVA) or the VO2 intercept (unloaded VO2) of the linear VO2-PVA relationship remained unchanged by fentanyl. Conclusions These results indicate that intracoronary fentanyl produces virtually no effects on LV mechanoenergetics for a wide range of its blood concentration.

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Normal distribution of ventricular pressure-volume area of arrhythmic beats under atrial fibrillation in canine heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00584.2004 ◽

2005 ◽

Vol 288 (4) ◽

pp. H1740-H1746 ◽

Cited By ~ 3

Author(s):

Satoshi Mohri ◽

Juichiro Shimizu ◽

Gentaro Iribe ◽

Haruo Ito ◽

Terumasa Morita ◽

...

Keyword(s):

Atrial Fibrillation ◽

Normal Distribution ◽

Frequency Distribution ◽

Mechanical Energy ◽

Systolic Pressure ◽

Left Ventricular ◽

Canine Heart ◽

Significance Level ◽

Nonnormal Distribution ◽

Skewness And Kurtosis

We previously found the frequency distribution of the left ventricular (LV) effective afterload elastance (Ea) of arrhythmic beats to be nonnormal or non-Gaussian in contrast to the normal distribution of the LV end-systolic elastance (Emax) in canine in situ LVs during electrically induced atrial fibrillation (AF). These two mechanical variables determine the total mechanical energy [systolic pressure-volume area (PVA)] generated by LV contraction when the LV end-diastolic volume is given on a per-beat basis. PVA and Emax are the two key determinants of the LV O2 consumption per beat. In the present study, we analyzed the frequency distribution of PVA during AF by its χ2, significance level, skewness, and kurtosis and compared them with those of other major cardiodynamic variables including Ea and Emax. We assumed the volume intercept (V0) of the end-systolic pressure-volume relation needed for Emax determination to be stable during arrhythmia. We found that PVA distributed much more normally than Ea and slightly more so than Emax during AF. We compared the χ2, significance level, skewness, and kurtosis of all the complex terms of the PVA formula. We found that the complexity of the PVA formula attenuated the effect of the considerably nonnormal distribution of Ea on the distribution of PVA along the central limit theorem. We conclude that mean (SD) of PVA can reliably characterize the distribution of PVA of arrhythmic beats during AF, at least in canine hearts.

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Effects of Intracoronary Fentanyl on Left Ventricular Mechanoenergetics in the Excised Cross-circulated Canine Heart

Anesthesiology ◽

10.1097/00000542-199706000-00017 ◽

1997 ◽

Vol 86 (6) ◽

pp. 1350-1358 ◽

Cited By ~ 6

Author(s):

Kunihisa Kohno ◽

Miyako Takaki ◽

Kazunari Ishioka ◽

Yasunori Nakayama ◽

Shunsuke Suzuki ◽

...

Keyword(s):

Oxygen Consumption ◽

Energy Use ◽

Mechanical Energy ◽

Systolic Pressure ◽

Left Ventricular ◽

Canine Heart ◽

Loading Conditions ◽

Wide Range ◽

Total Mechanical Energy ◽

Lv Volumes

Background It is still unclear whether fentanyl directly alters left ventricular (LV) contractility and oxygen consumption. This is because of the difficulty in defining and evaluating contractility and energy use independently of ventricular loading conditions and heart rate in beating whole hearts. Methods This study was conducted to clarify the mechanoenergetic effects of intracoronary fentanyl in six excised cross-circulated canine hearts. The authors used the framework of the E(max) (a contractility index)-PVA (systolic pressure-volume area, a measure of total mechanical energy)-VO2 (myocardial oxygen consumption per beat) relationship practically independent of ventricular loading conditions. The authors measured LV pressure, volume, coronary flow, and arteriovenous oxygen content difference to calculate E(max), PVA, and VO2. They first obtained the VO2-PVA relationship for varied LV volumes at control E(max). The authors then obtained the VO2-PVA relationship at a constant LV volume, whereas coronary blood fentanyl concentration was increased in steps up to 240 ng/ml. Finally, they obtained the VO2-PVA relationship for varied LV volumes at the final dose of fentanyl. Results Fentanyl at any concentrations did not significantly change E(max), PVA, and VO2 from the control. The linear end-systolic pressure-volume relations and their slopes were virtually the same between the control and fentanyl volume loading in each heart. Further, either the slope (oxygen cost of PVA) or the VO2 intercept (unloaded VO2) of the linear VO2-PVA relationship remained unchanged by fentanyl. Conclusions These results indicate that intracoronary fentanyl produces virtually no effects on LV mechanoenergetics for a wide range of its blood concentration.

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Mechanoenergetics of the Negative Inotropism of Isoflurane in the Canine Left Ventricle

Anesthesiology ◽

10.1097/00000542-199707000-00012 ◽

1997 ◽

Vol 87 (1) ◽

pp. 82-93 ◽

Cited By ~ 14

Author(s):

Yasunori Nakayama ◽

Miyako Takaki ◽

Kunihisa Kohno ◽

Junichi Araki ◽

Hiroyuki Suga

Keyword(s):

Oxygen Consumption ◽

Myocardial Oxygen Consumption ◽

Mechanical Energy ◽

Contractile Proteins ◽

Left Ventricular ◽

Free Calcium ◽

Canine Heart ◽

Inotropic Effects ◽

Total Mechanical Energy ◽

Lv Volume

Background The mechanisms underlying the negative inotropic effects of isoflurane are incompletely understood. One suggested mechanism is that isoflurane may decrease Ca2+ sensitivity of contractile proteins. If so, more free calcium would be needed to activate contractile proteins to the same degree, which would impose a greater requirement for myocardial oxygen consumption used in the cycling of calcium. In this study, the authors use the excised, cross-circulated, canine heart model and the volume servopump technique to measure the effects of isoflurane on Emax (a contractile index) and on the relationship between pressure-volume area (PVA, a measure of total mechanical energy) and myocardial oxygen consumption per beat (VO2). Methods Effects of intracoronary isoflurane infused via a precoronary oxygenator on myocardial mechanoenergetics were studied during isovolumic contractions. The authors measured left ventricular (LV) pressure, LV volume, coronary flow, and arteriovenous oxygen content difference and computed Emax, VO2 and PVA at 0, 1.0, 1.5, and 2.0% isoflurane. From these data, the authors obtained oxygen costs of PVA and Emax in control subjects and in those receiving 2.0% isoflurane. Results Emax, PVA, and VO2 dose-dependently decreased by similar degrees (P < 0.05). Isoflurane did not change the oxygen costs at 1.5% and 2.0% concentration (P < 0.05). Conclusions These mechanoenergetic findings suggest that the primary method by which isoflurane decreases contractility is not by decreasing Ca2+ sensitivity of contractile proteins but mainly by decreasing Ca2+ handling in the excitation-contraction coupling without myocardial oxygen wasting effect.

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Left ventricular O2 consumption and pressure-volume area in puppies

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.4.h770 ◽

1987 ◽

Vol 253 (4) ◽

pp. H770-H776 ◽

Cited By ~ 1

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.

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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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