Biomedical subjects

O Kawaguchi

Publications and source records attributed to O Kawaguchi.

At least 55 records · Page 3Linked to original sources

PubMed1993

Ventricular perspective on efficiency.

The heart has many efficiencies of different definitions, of which mechanical work efficiency is the most popular and conventional. We have proposed a method to quantify the total mechanical energy generated by ventricular contraction. This energy can be quantified as a specific area called "systolic pressure-volume area" or "PVA" in the ventricular pressure-volume diagram. In the left ventricle of excised, cross-circulated dog heart preparations, we found a closely linear relation between PVA and oxygen consumption (VO2) under various loading conditions in a stable contractile state (Emax). An enhanced contractility was accompanied by an elevation of the load-independent VO2-PVA relation in a parallel manner, where the elevation was proportional to Emax. The slope of the VO2-PVA relation represents the "oxygen cost of mechanical energy (or PVA)" and its reciprocal indicates the "contractile efficiency", i.e., the energy conversion efficiency from PVA-dependent VO2 to PVA. This efficiency was 40% on the average, independent of various inotropic interventions. The slope of the PVA-independent VO2-Emax relation represents the "oxygen cost of contractility (or Emax)". This cost was relatively constant for different inotropic interventions except for myocardial cooling and stunning. We considered the discrepancy between the stable contractile efficiency and the variable thermal economy of force generation and maintenance.

Animals↗

PubMed1993

Determinants of myocardial oxygen consumption in fibrillating dog hearts. Comparison between normothermia and hypothermia.

The purpose of the present study was to elucidate the mechanism of the difference in myocardial oxygen consumption between heating and fibrillating states during normothermia and hypothermia. In five isolated cross-circulated dog hearts, we measured left ventricular pressure at several ventricular volumes and myocardial oxygen consumption at V0 and V100, at which peak isovolumic pressures were zero and approximately 100 mm Hg, respectively, in beating and fibrillating states during normothermia and hypothermia (29 degrees C). As a measure of the total mechanical energy at V100, we obtained pressure-volume area in the beating state and equivalent pressure-volume area for fibrillation. We calculated equivalent heart rate as an estimate of the contraction frequency of individual myocytes in a fibrillating ventricle from myocardial oxygen consumption at V0 in the beating and fibrillating states. During normothermia, myocardial oxygen consumption per minute at V0 and V100 and myocardial oxygen consumption for mechanical purposes at V100 (myocardial oxygen consumption at V100-myocardial oxygen consumption at V0) were significantly higher during fibrillation than in the beating state. Equivalent pressure-volume area during fibrillation and pressure-volume area in the beating state at V100 were comparable, whereas equivalent heart rate during fibrillation was significantly higher than heart rate in the beating state. During hypothermia, myocardial oxygen consumption was comparable between beating and fibrillating states at V0, although myocardial oxygen consumption at V100 was slightly lower during fibrillation than in the beating state. Myocardial oxygen consumption for mechanical purposes during fibrillation was half of that in the beating state. Equivalent pressure-volume area was significantly smaller than pressure-volume area, whereas equivalent heart rate and heart rate were comparable. We conclude that during normothermia, higher myocardial oxygen consumption during fibrillation than in the beating state at V0 and V100 is attributable to the higher contraction frequency. During hypothermia the comparable myocardial oxygen consumption values at V0 are attributable to the comparable contraction frequencies, whereas slightly lower myocardial oxygen consumption during fibrillation at V100 is ascribed to the lower total mechanical energy.

Animals↗

PubMed1992

Ejecting volume, filling volume and stroke volume gains: new indexes of inotropism and lusitropism.

We propose new indexes to evaluate the effects of ventricular inotropism and lusitropism on stroke volume. The end-systolic pressure-volume relationship (ESPVR) or its slope (Emax) has been employed to assess ventricular inotropism. The end-diastolic pressure-volume relationship (EDPVR) or compliance has been used to express ventricular diastolic properties or lusitropism. However, their net effect on stroke volume under a given set of preload and afterload pressures has not quantitatively been evaluated. Ejecting volume gain (Ge) was proposed to quantify the inotropic effect on stroke volume by the change in end-systolic volume between the two ESPVR curves obtained before and during an inotropic intervention at a specified ejecting pressure. Ge is a function of afterload pressure. Filling volume gain (Gf) was proposed to quantify the lusitropic effect on stroke volume by the change in end-diastolic volume between the two EDPVR curves before and during a lusitropic intervention at a specified filling pressure. Gf is a function of preload pressure. The net effect of these inotropic and lusitropic effects on stroke volume at these specified preload and afterload pressures can be expressed by the sum of Ge and Gf. We call this sum stroke volume gain (Gsv). Gsv is a function of preload and afterload pressures. Using representative examples, we demonstrate that these new indexes are conceptually useful to quantitatively understand changes in the pumping ability of the heart under simultaneous inotropic and lusitropic effects as a function of ejecting and filling pressures.

Animals↗

PubMed1992

Epinephrine and calcium have similar oxygen costs of contractility.

We compared the oxygen cost of increasing ventricular contractility using Emax (slope of the ventricular end-systolic pressure-volume relation) as the index of ventricular contractility. Contractility was enhanced by calcium and epinephrine in paired experiments on dog left ventricles. Firstly, we obtained left ventricular oxygen consumption (VO2) and systolic pressure-volume area (PVA, a measure of total mechanical energy) of contractions at different volumes in the control contractile state to determine a reference VO2-PVA relation. PVA was obtained as the area in the pressure-volume (P-V) diagram which was bounded by the end-systolic P-V line, end-diastolic P-V curve and systolic P-V trajectory of individual contractions. Secondly, we gradually enhanced Emax with calcium and epinephrine in two consecutive runs at a fixed ventricular volume. Both VO2 and PVA increased with enhanced Emax. From these VO2-PVA data, we calculated the PVA-independent VO2 values at the respective enhanced Emax levels and determined the oxygen cost of Emax as the slope of the relation between the PVA-independent VO2 and Emax. The cost per beat and per 100 g was 0.00158 ml O2/(mmHg/ml) for calcium and 0.00166 ml O2/(mmHg/ml) for epinephrine on average, values not significantly different from each other (P less than 0.05). We conclude that epinephrine and calcium have similar oxygen costs of contractility over a wide range of Emax despite their different pharmacological mechanisms of positive inotropism.

Animals↗

PubMed1992

Comparable efficiencies of chemomechanical energy transduction between beating and fibrillating dog hearts.

We have recently proposed a mechanical index, equivalent pressure-volume (PV) area (ePVA), as a measure of the total mechanical energy during ventricular fibrillation (VF). ePVA, an analogue of the PV area (PVA) of a beating heart, is the area surrounded by the isobaric line drawn at the VF pressure, the end-systolic and end-diastolic PV relations of the beating state. In the present study, using a closed-air chamber system, we actually produced isobaric contractions, PVAs of which were identical with ePVAs during VF. Myocardial O2 consumption (VO2) during VF was measured and compared with the estimated value from VO2 of isobaric contraction with identical PVA and equivalent heart rate (eHR). eHR, an estimate of the contraction frequency of each myocyte during VF, was determined from unloaded VO2 in beating and fibrillating states. The efficiency of the energy conversion from VO2 for mechanical purposes to the total mechanical energy (contractile efficiency) during VF was calculated as the reciprocal of the slope of the VO2-ePVA relation. The estimated VO2 during VF agreed with measured VO2 (r = 0.96, regression coefficient = 1.13). The slope of the VO2-ePVA relation during VF was not different from that in the beating state in all hearts by analysis of covariance, and mean contractile efficiency during VF (51 +/- 23%) was not significantly different from that in the beating state (40 +/- 12%). We conclude that 1) ePVA is considered to represent the total mechanical energy during VF, and 2) contractile efficiency during VF is comparable to that in the beating state.

Animals↗

PubMed1992

Mechanoenergetic effects of pimobendan in canine left ventricles. Comparison with dobutamine.

BACKGROUND: We hypothesized that the effect of pimobendan (UD-CG 115 BS) to increase calcium sensitivity of contractile protein might result in less myocardial oxygen consumption (VO2) in comparison with dobutamine when they enhance ventricular contractility to the same extent. To examine this hypothesis, we compared the effects of pimobendan and dobutamine on left ventricular contractility and energetics using the frameworks of Emax (contractility index) and the relation between VO2 and PVA (systolic pressure-volume area, a measure of left ventricular total mechanical energy). METHODS AND RESULTS: We measured VO2, Emax, PVA, and force-time integral (FTI) in excised, cross-circulated, nonfailing dog hearts. The slope of the VO2-PVA relation reciprocally indicates the efficiency from PVA-dependent VO2 to the total mechanical energy (contractile efficiency). The VO2 intercept of the VO2-PVA relation, i.e., PVA-independent VO2, reflects energy utilization for excitation-contraction coupling. The ratio of FTI to PVA-dependent VO2 can be called contractile economy. Both drugs comparably enhanced Emax. Although the contractile economy was greater by 14 +/- 19% (p less than 0.05) for pimobendan than for dobutamine, the contractile efficiency was similar between the two drugs. Oxygen cost of contractility, defined as the slope of the relation between the PVA-independent VO2 and Emax, was the same between the two drugs. Other mechanoenergetic effects of both drugs were similar except for a greater coronary vasodilating effect of pimobendan. CONCLUSIONS: Pimobendan has almost the same mechanoenergetic effects as dobutamine but slightly greater contractile economy and coronary vasodilation. The calcium-sensitizing effect of pimobendan did not save the oxygen cost of contractility.

Animals↗

PubMed1992

Left ventricular contractility and energetic cost in disease models--an approach from the pressure-volume diagram.

Left ventricular contractility and the energetic cost of contraction were assessed in various disease models in experimental animals utilizing frameworks of Emax (left ventricular contractility index) and pressure-volume area (PVA, a measure of total left ventricular mechanical energy expenditure) derived from the pressure-volume (P-V) diagram. Under various contractile conditions, PVA linearly correlates with myocardial oxygen consumption per beat (VO2) in a load-independent manner. The reciprocal of the slope of the linear VO2-PVA relation indicates "contractile efficiency" (the energy transduction efficiency from oxygen to total mechanical energy). It was similar between dog and rabbit hearts (about 40%) and was not significantly affected by enhanced contractility with calcium, epinephrine, or cardiac cooling, or by depressed contractility with propranolol, decreased coronary perfusion pressure, or stunned myocardium. However, in thyrotoxic rabbit hearts contractile efficiency was significantly depressed compared to normal hearts. On the other hand, the VO2 intercept of the VO2-PVA relation (PVA-independent VO2), which reflects VO2 for non-mechanical activities such as excitation-contraction coupling and basal metabolism, positively correlates with Emax. Therefore, the ratio of an increase in PVA-independent VO2 to an increase in Emax indicates "oxygen cost of contractility". Oxygen cost of contractility was higher in stunned myocardium than in normal hearts, suggesting that the energy cost of calcium handling is elevated in stunned myocardium. Thus, using the frameworks of Emax and PVA, we can interconnect cardiac mechanics and energetics. Further, using the concepts of contractile efficiency and oxygen cost of contractility, we can approach the pathogenesis of variously altered contractile conditions.

Animals↗

PubMed1992

Myocardial oxygen consumption of fibrillating ventricle in hypothermia. Successful account by new mechanical indexes--equivalent pressure-volume area and equivalent heart rate.

We studied the effects of cardiac hypothermia on myocardial oxygen consumption of a fibrillating ventricle and evaluated whether myocardial oxygen consumption of a fibrillating ventricle in hypothermia can be accounted for by new mechanical indexes: equivalent pressure-volume area and equivalent heart rate in the isolated cross-circulated canine heart preparation. Equivalent pressure-volume area is the area that is surrounded by a horizontal pressure-volume line at the pressure of a fibrillating ventricle and the end-systolic and end-diastolic pressure-volume relations in the beating state in the pressure-volume diagram. Equivalent pressure-volume area is an analog of the pressure-volume area of a beating heart and has been proposed to be a measure of the total mechanical energy of a fibrillating ventricle. Equivalent heart rate was calculated from myocardial oxygen consumption per minute in both beating and fibrillating states under unloaded conditions as an estimate of the frequency of contractions of individual myocytes on the assumption that individual myocytes during ventricular fibrillation have the same contractility as that in the beating state. We estimated myocardial oxygen consumption per minute of the fibrillating ventricle at various ventricular volumes as a function of both equivalent pressure-volume area and equivalent heart rate. The myocardial oxygen consumption-equivalent pressure-volume area relation during ventricular fibrillation in hypothermia was highly linear, with a correlation coefficient of 0.90 (mean). The relation between estimated and directly measured myocardial oxygen consumption values of a fibrillating ventricle in hypothermia was highly linear (r = 0.98), and the regression line (y = 0.80x + 0.48) was close to the identity line in the working range. Therefore we conclude that equivalent pressure-volume area is the primary determinant of myocardial oxygen consumption during ventricular fibrillation in hypothermia, and myocardial oxygen consumption of a fibrillating ventricle in hypothermia can be accounted for by the combination of equivalent pressure-volume area and equivalent heart rate as in normothermia.

Animals↗

PubMed1992

Energetics of the fibrillating ventricle.

We have proposed a new mechanical index, equivalent pressure-volume area (ePVA), as a measure of the total mechanical energy of a fibrillating ventricle. ePVA is an analogue of the pressure-volume area (PVA) of a contracting ventricle and the specific area surrounded by the horizontal pressure-volume line at the pressure of ventricular fibrillation (VF) and the end-systolic and end-diastolic pressure-volume relations in the beating state in the pressure-volume diagram. In the isolated, cross-circulated heart preparation, we obtained myocardial oxygen consumption (VO2) during VF and ePVA at various left ventricular volumes in the control, epinephrine, propranolol and hypothermia runs. ePVA was highly linearly correlated with VO2 in all runs (r = 0.95, 0.98, 0.96 and 0.90, respectively). We also determined equivalent heart rate (eHR) as an estimate of the contraction frequency of individual myocytes in a fibrillating ventricle from mechanically unloaded VO2 in beating and fibrillating states. Using both ePVA and eHR, VO2 during VF was estimated and correlated with directly measured VO2. Estimated VO2 almost agreed with measured VO2 in all runs. We conclude that ePVA is a primary determinant of VO2 during VF, and that VO2 of a fibrillating ventricle can be reasonably accounted for by the combination of ePVA and eHR. This paper is a review of our previous studies on the energetics of a fibrillating ventricle.

Animals↗

PubMed1992

Ventricular fibrillation does not depress postfibrillatory contractility in blood-perfused dog hearts.

We studied whether ventricular fibrillation depresses ventricular contractility in a blood-perfused heart. In 12 excised, cross-circulated dog hearts, we measured left ventricular pressure and myocardial oxygen consumption at a middle left ventricular volume as control and induced ventricular fibrillation electrically. Six hearts were subjected to 20 minutes of ventricular fibrillation (group A), and the other six hearts were subjected to 40 minutes of ventricular fibrillation (group B). Then we defibrillated the heart with direct current shock and measured left ventricular pressure, left ventricular volume, and myocardial oxygen consumption immediately, 10 minutes, 20 minutes, and 30 minutes after the defibrillation. Coronary perfusion pressure was maintained normal (around 100 mm Hg) by the arterial pressure of the support dog throughout each experiment. Ventricular contractility was quantified by the maximum value for the instantaneous pressure/volume ratio (Emax). Pooled data of both groups A and B showed that Emax immediately after defibrillation increased to 116% +/- 28% (p less than 0.05) of control level and Emax 10 minutes after defibrillation decreased to 84% +/- 17% (p less than 0.05) of control level. Then Emax recovered to the control level: 95% +/- 18% (p greater than 0.05) of control level at 20 minutes and 100% +/- 20% (p greater than 0.05) of control level at 30 minutes after defibrillation. Emax of group A was not different from that of group B at comparable measurement times after defibrillation. Changes in myocardial oxygen consumption per beat were in proportion to the changes in Emax. We conclude that ventricular fibrillation per se for 20 to 40 minutes does not depress postfibrillatory contractility when coronary blood perfusion is maintained normal in the dog left ventricle.

Animals↗

PubMed1992

Mechanical enhancement and myocardial oxygen saving by synchronized dynamic left ventricular compression.

Dynamic cardiomyoplasty with synchronously paced skeletal muscle grafts has recently been developed to augment the performance of impaired myocardium. This method has been reported effective to improve patients' general status and some hemodynamic parameters. It is unknown, however, how a systolic dynamic cardiac compression, as in dynamic cardiomyoplasty, affects left ventricular energetics. The purpose of this study was to characterize the effects of dynamic cardiac compression on the ventricle in terms of the pressure-volume relationship and myocardial oxygen consumption. In an isolated cross-circulated dog heart model, a dynamic cardiac compression device was set to directly compress the ventricle during systole. End-systolic pressure, contractility index (Emax), pressure-volume area, external mechanical work, coronary blood flow, and myocardial oxygen consumption were determined before and during dynamic cardiac compression. Dynamic cardiac compression significantly increased Emax. When end-diastolic and stroke volumes were fixed, end-systolic pressure, pressure-volume area, and external mechanical work significantly increased during dynamic cardiac compression while coronary blood flow and myocardial oxygen consumption remained unchanged. When end-systolic pressure was matched with the pre-dynamic cardiac compression control level by decreasing end-diastolic volume at a constant stroke volume so that external mechanical work under dynamic cardiac compression returned to the control level, both pressure-volume area and myocardial oxygen consumption significantly decreased. In contrast to a marked increase in myocardial oxygen consumption for a given increase in external mechanical work by either volume loading or dobutamine, dynamic cardiac compression did not increase myocardial oxygen consumption for the same increase in external mechanical work. Thus dynamic cardiac compression augments left ventricular pump function without increasing myocardial oxygen demand or compromising coronary blood flow.

Animals↗

PubMed1991

Systolic pressure-volume area (PVA) as the energy of contraction in Starling's law of the heart.

We have theoretically proposed "systolic pressure-volume area" (PVA) as a measure of total mechanical energy generated by ventricular contraction. We then experimentally showed that PVA closely correlates with left ventricular oxygen consumption (Vo2) regardless of ventricular loading conditions in a stable contractile state. Although Starling's law of the heart has been generally considered to describe the relation between ventricular preload as the input and the "energy of contraction" as the output, the energy of cardiac contraction has been variously identified with cardiac output, external work, contractile element work, tension-time index, etc., by different investigators. However, none of these variables has been unanimously accepted as the total mechanical energy of contraction because they do not consistently correlate with Vo2 which represents the total energy utilization for contraction. Considering the nature of PVA which has been revealed over the last decade, we now confidently propose that PVA is the most likely expression of the total mechanical energy of contraction that has been pursued for many years as the energy of contraction in Starling's law of the heart.

Blood Pressure↗

PubMed1991

Multicompartment model for mechanics and energetics of fibrillating ventricle.

We propose a new mechanical model of a fibrillating ventricle to interrelate ventricular mechanics and energetics during fibrillation. The model consists of multiple asynchronously contracting compartments with identical time-varying elastances but with different contraction phase lags. Pressures in all compartments are common, and volumes of all compartments change, keeping their sum constant in the model. We evaluated the mechanical behavior of each compartment by simulating this model on a personal computer. Results showed that each compartment contracts quasi-isobarically. We calculated the pressure-volume area (PVAc) of each compartment as a measure of the total mechanical energy generated by a contraction of the compartment. We found that the sum of PVAcs of all compartments agreed with the area (equivalent PVA; ePVA) surrounded by the end-systolic and end-diastolic pressure-volume relations and the isobaric line at the mean pressure of the fibrillating ventricle. We conclude that ePVA represents the total mechanical energy of the fibrillating ventricle model. The multicompartment model is useful for insight into the interrelation between ventricular mechanics and energetics during ventricular fibrillation.

Animals↗

PubMed1991

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

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.

Animals↗

PubMed1991

Increased oxygen cost of contractility in stunned myocardium of dog.

Recent studies have shown that myocardial oxygen consumption does not proportionally decrease with the deterioration of contractile function in stunned myocardium. To investigate this disproportion, we studied the end-systolic pressure-volume relation and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA, a measure of total mechanical energy) in stunned hearts. In the VO2-PVA relation, VO2 can be divided into PVA-dependent and PVA-independent fractions. In excised cross-circulated dog left ventricles, a 15-minute normothermic global ischemia followed by 60-120 minutes of reperfusion significantly decreased the ventricular contractility index (Emax) by approximately 40%, but the PVA-independent VO2 did not significantly decrease. Oxygen cost of PVA, defined as the slope of the VO2-PVA relation, was slightly decreased in stunned hearts. Restoration of the depressed Emax to the preischemic control level by calcium infusion increased the PVA-independent VO2 to 137 +/- 27% of control level (p less than 0.01). Oxygen cost of contractility, defined as the slope of the relation between PVA-independent VO2 and Emax, increased from 0.0011 +/- 0.0003 to 0.0023 +/- 0.0005 ml O2.ml.mm Hg-1.beat-1 per 100 g myocardium in control and stunned hearts, respectively (p less than 0.01). From these new finding, we conclude that the unchanged VO2, despite the depressed contractility in stunned myocardium, is mainly due to the increased oxygen cost of contractility.

Animals↗

PubMed1991

Denopamine (beta 1-selective adrenergic receptor agonist) and isoproterenol (non-selective beta-adrenergic receptor agonist) equally increase heart rate and myocardial oxygen consumption in dog heart.

The effects of denopamine (a beta 1-selective adrenergic receptor agonist) and isoproterenol (a non-selective beta-adrenergic receptor agonist) on heart rate, left ventricular contractility, and left ventricular oxygen consumption (VO2) at the same left ventricular volume were compared in excised cross-circulated dog hearts. Denopamine and isoproterenol increased heart rate and VO2 to a comparable extent at a comparably increased contractility. Moreover, the oxygen cost of contractility which quantifies VO2 for excitation-contraction coupling was the same between the two agents. These findings contradict the previously reported smaller increases in heart rate and VO2 by denopamine than by isoproterenol in open-chest dog hearts, which have been mainly attributed to the beta 1-selectivity of denopamine. Our results suggest that in isolated and denervated hearts, the degree of beta 1-selectivity of a beta-agonistic agent does not directly determine the relative potencies of its inotropic and chronotropic effects and the oxygen cost of contractility.

Adrenergic beta-Agonists↗

PubMed1991

Calcium kinetics and energetics in myocardium. Simulation study.

We carried out a simulation study to obtain insight into the relation between calcium (Ca2+) transients and energy for handling Ca2+ in excitation-contraction (EC) coupling. The simulation incorporated basic Ca2+ kinetics among total released Ca2+ from sarcoplasmic reticulum (SR), myoplasmic free Ca2+ ion concentration, and troponin (Tn)-Ca complex concentration ([TnCa]). The total Ca2+ released from the SR was arbitrarily set as an impulse and three rate constants were used for Ca2+ binding to Tn, Ca2+ dissociation from Tn, and Ca2+ uptake by SR. The results showed that the peak Ca2+ transient varies widely as a reciprocal of the Ca2+ sensitivity of the contractile machinery, despite constant total released Ca2+ and hence, a constant energy for Ca2+ handling. This result suggests a disproportate relationship between the magnitude of Ca2+ transients and the energy for Ca2+ handling when the Ca2+ sensitivity of contractile machinery changes.

Calcium↗

PubMed1991

Equivalent heart rate during ventricular fibrillation in the dog heart: mechanoenergetic analysis.

We propose equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual myocytes in a fibrillating ventricle by analyzing mechanics and energetics of the ventricle. Using the isolated, cross-circulated dog heart preparation, we determined eHR in two different ways. First, we obtained eHR (eHR1) from myocardial O2 consumption (Vo2)-equivalent pressure-volume area (ePVA) data points during ventricular fibrillation (VF) by utilizing the Vo2-pressure-volume area (PVA) relation in the beating state. PVA is the area surrounded by the end-systolic and end-diastolic pressure-volume relations and the systolic pressure-volume trajectory in the pressure-volume diagram. PVA has been shown to represent the total mechanical energy generated by each contraction. We have recently proposed ePVA as a measure of the total mechanical energy generated by single contractions of all individual asynchronously contracting myocytes in a fibrillating ventricle. ePVA is the area surrounded by the horizontal line at the VF pressure and the end-systolic and end-diastolic pressure-volume relations in the beating state. Second, we measured Vo2 in beating state at various heart rates and Vo2 during VF under a mechanically unloaded condition. By comparing these fibrillating and beating Vo2 values, we determined eHR (eHR2) for the fibrillating state. eHR1 was 216 +/- 27 beats/min and eHR2 was 223 +/- 26 beats/min. These two values were not significantly different. We conclude that the average frequency of contractions of individual myocytes in a fibrillating ventricle is equivalent approximately to 220 beats/min in terms of ventricular energetics.

Animals↗