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.

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.

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.

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.

O2 consumption of dog heart under decreased coronary perfusion and propranolol

1988 ◽  
Vol 254 (2) ◽  
pp. H292-H303 ◽  
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.

Hemodynamic and mechanical determinants of myocardial O2 consumption in normal human heart: effects of dobutamine

1993 ◽  
Vol 265 (6) ◽  
pp. H1884-H1892 ◽  
Author(s):  
J. L. Vanoverschelde ◽  
W. Wijns ◽  
B. Essamri ◽  
A. Bol ◽  
A. Robert ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Rate Pressure Product ◽  
O2 Consumption ◽  
Ventricular Ejection Fraction ◽  
Pressure Work ◽  
Work Index ◽  
Myocardial O2 Consumption

The relationship of myocardial O2 consumption (MVO2) to its potential hemodynamic and mechanical determinants was investigated in eight healthy normal volunteers at rest and during infusion of dobutamine (5–10 micrograms.kg-1.min-1). MVO2 was calculated from the monoexponential myocardial clearance of [1–11C]acetate with positron emission tomography, and left ventricular mechanical function was assessed by two-dimensional echocardiography. Infusion of dobutamine increased heart rate by 53%, the tension-time index by 31%, and the rate-pressure product by 116%. Cardiac output (+70%), left ventricular ejection fraction (+24%), total mechanical energy [systolic pressure-volume area, (PVA) +84%], and left ventricular pressure-work index (+100%) also increased during infusion of dobutamine. During infusion of dobutamine, MVO2 increased from 96 +/- 17 to 233 +/- 19 J.min-1.100 g left ventricle-1, while myocardial efficiency (the ratio of PVA to MVO2) decreased from 46 +/- 8 to 35 +/- 4% (P < 0.001 each). MVO2 was best correlated (P < 0.001) with the PVA (r = 0.92) and the pressure-work index (r = 0.92). Infusion of dobutamine also resulted in a significant parallel upward shift of the PVA-MVO2 relationship, indicative of an increase in PVA-independent MVO2. Our data indicate that, in human subjects, MVO2 is mainly related to systolic PVA and that inotropic stimulation with dobutamine results in decreased efficiency of contraction, such as that previously described in isolated hearts.

NHE-1 participates in isoproterenol-induced downregulation of SERCA2a and development of cardiac remodeling in rat hearts

2011 ◽  
Vol 301 (5) ◽  
pp. H2154-H2160 ◽  
Author(s):  
Munetaka Shibata ◽  
Daisuke Takeshita ◽  
Koji Obata ◽  
Shinichi Mitsuyama ◽  
Haruo Ito ◽  
...  
Keyword(s):  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Beneficial Effects ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Male Wistar Rats ◽  
Lv Volume

Impaired Ca2+ handling is one of the main characteristics in heart failure patients. Recently, we reported abnormal expressions of Ca2+-handling proteins in isoproterenol (ISO)-induced hypertrophied rat hearts. On the other hand, Na+/H+ exchanger (NHE)-1 inhibitor has been demonstrated to exert beneficial effects in ischemic-reperfusion injury and in the development of cardiac remodeling. The aims of the present study are to investigate the role of NHE-1 on Ca2+ handling and development of cardiac hypertrophy in ISO-infused rats. Male Wistar rats were randomly divided into vehicle [control (CTL)] and ISO groups without or with pretreatment with a selective NHE-1 inhibitor, BIIB-723. ISO infusion for 1 wk significantly increased the ratios of heart to body weight and left ventricle (LV) to body weight and collagen accumulation. All of these increases were antagonized by coadministration with BIIB-723. The ISO-induced significant increase in LV wall thickness was suppressed significantly ( P < 0.05) by BIIB-723. ISO-induced decreases in cardiac stroke volume and a total mechanical energy per beat index, systolic pressure-volume area at midrange LV volume, were normalized by BIIB-723. The markedly higher expression of NHE-1 protein in the ISO group than that in CTL group was suppressed ( P < 0.05) by BIIB-723. Surprisingly, ISO induced downregulation of the important Ca2+-handling protein sarcoplasmic reticulum Ca2+-ATPase 2a, the expression of which was also normalized by BIIB-723 without changes in phosphorylated phospholamban (PLB)/PLB expression. We conclude that NHE-1 contributes to ISO-induced abnormal Ca2+ handling associated with cardiac hypertrophy. Inhibition of NHE-1 ameliorates cardiac Ca2+-handling impairment and prevents the development of cardiac dysfunction in ISO-infused rats.

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of α-fodrin

2001 ◽  
Vol 281 (3) ◽  
pp. H1286-H1294 ◽  
Author(s):  
Tsuyoshi Tsuji ◽  
Yoshimi Ohga ◽  
Yoshiro Yoshikawa ◽  
Susumu Sakata ◽  
Takehisa Abe ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Calpain Inhibitor ◽  
Contractile Dysfunction ◽  
Area Index ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Total Mechanical Energy ◽  
Cardiac Contractile Dysfunction ◽  
Contractile Failure

The aim of the present study was to examine the mechanisms of Ca2+ overload-induced contractile dysfunction in rat hearts independent of ischemia and acidosis. Experiments were performed on 30 excised cross-circulated rat heart preparations. After hearts were exposed to high Ca2+, there was a contractile failure associated with a parallel downward shift of the linear relation between myocardial O2 consumption per beat and systolic pressure-volume area (index of a total mechanical energy per beat) in left ventricles from all seven hearts that underwent the protocol. This result suggested a decrease in O2consumption for total Ca2+ handling in excitation-contraction coupling. In the hearts that underwent the high Ca2+ protocol and had contractile failure, we found marked proteolysis of a cytoskeleton protein, α-fodrin, whereas other proteins were unaffected. A calpain inhibitor suppressed the contractile failure by high Ca2+, the decrease in O2 consumption for total Ca2+ handling, and membrane α-fodrin degradation. We conclude that the exposure to high Ca2+ may induce contractile dysfunction possibly by suppressing total Ca2+ handling in excitation-contraction coupling and degradation of membrane α-fodrin via activation of calpain.

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.

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

1983 ◽  
Vol 244 (2) ◽  
pp. H206-H214 ◽  
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.

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

1997 ◽  
Vol 87 (3) ◽  
pp. 658-666 ◽  
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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