Biomedical subjects

O Kawaguchi

Publications and source records attributed to O Kawaguchi.

At least 19 recordsLinked to original sources

PubMed1997

Dynamic cardiac compression improves contractile efficiency of the heart.

The effect of dynamic cardiac compression on left ventricular contractile efficiency was assessed in terms of the pressure-volume relationship and myocardial oxygen consumption. In 11 excised cross-circulated dog hearts, the ventricle was directly compressed during systole (dynamic cardiac compression). Measurements for pressure-volume area (a measure of total mechanical energy), external work, and myocardial oxygen consumption were done before and during dynamic cardiac compression. Dynamic cardiac compression increased pressure-volume area by 28% +/- 17% (mean plus or minus the standard deviation) and external work by 24% +/- 20% (p = 0.0000185 and 0.0000212, respectively) at given end-diastolic and stroke volumes without affecting myocardial oxygen consumption. As a result, the oxygen cost of pressure-volume area, that is, the slope of the myocardial oxygen consumption-pressure-volume area relationship, significantly decreased by 16% +/- 13% (p = 0.0000135) whereas the pressure-volume area-independent myocardial oxygen consumption was unchanged. Then, contractile efficiency, that is, the reciprocal of the slope of the myocardial oxygen consumption-pressure-volume area relationship in joules significantly improved from 45% +/- 8% to 53% +/- 13% (p = 0.0000437). When the native myocardial oxygen consumption-pressure-volume area relationship was assessed by subtracting the dynamic cardiac compression pressure applied to the heart, the slope of the myocardial oxygen comsumption-pressure-volume area relationship returned to the control level. This indicates that the contractile efficiency of the native heart was not affected by dynamic cardiac compression. We conclude that dynamic cardiac compression enhances left ventricular pump function by improving the contractile efficiency of the overall heart leaving the energetics of the native heart unchanged.

Animals↗

PubMed1996

Bidirectional augmentation of heart rate regulation by autonomic nervous system in rabbits.

Although the characteristics of the static interaction between the sympathetic and parasympathetic nervous systems in regulating heart rate (HR) have been well established, how the dynamic interaction modulates the HR response remains unknown. We therefore investigated dynamic interaction by estimating the transfer function from nerve stimulation to HR using a band-limited Gaussian white-noise technique. The transfer function relating dynamic sympathetic stimulation to HR had characteristics of a second-order low-pass filter. Simultaneous tonic vagal stimulation at 5 and 10 Hz increased gain of the transfer function by 55.0 +/- 40.1 and 80.7 +/- 50.5%, respectively (P < 0.05). The transfer function from dynamic vagal stimulation to HR had characteristics of a first-order low-pass filter. Simultaneous tonic sympathetic stimulation at 5 and 10 Hz increased the gain by 18.2 +/- 17.9 and 24.1 +/- 18.0%, respectively (P < 0.05). Thus interaction augmented dynamic gain bidirectionally, even though it affected mean HR antagonistically. By virtue of this interaction, the autonomic nervous system appears to extend its dynamic range of operation.

Animals↗

PubMed1996

Neural arc of baroreflex optimizes dynamic pressure regulation in achieving both stability and quickness.

The baroreflex loop consists of a fast neural arc and a slow mechanical arc. We hypothesized that the neural baroreflex arc compensates the slow mechanical response and thus improves the quality of blood pressure regulation. We estimated the open-loop transfer characteristics of the neural baroreflex arc (HP), i.e., from carotid sinus pressure to sympathetic nerve activity (SNA), and that of the effective peripheral baroreflex arc (Hp), i.e., from SNA to arterial pressure, in anesthetized rabbits. The gain of Hn was constant below 0.12 +/- 0.057 Hz and increased with a slope of 6.1 +/- 0.06 dB/octave above its frequency up to 1 Hz. In contrast, the gain of Hp was constant below 0.071 +/- 0.03 Hz and decreased with a slope of -11.0 +/- 1.48 dB/octave above the frequency. These data indicate that Hn accelerates slow peripheral responses in the frequency range of 0.1-1 Hz. Although too much acceleration in the high-frequency range could result in instability of the system, numerical analysis of the closed-loop baroreflex response indicated that the neural arc optimized arterial pressure regulation in achieving both stability and quickness.

Animals↗

PubMed1995

Left ventricular mechanoenergetics during asynchronous left atrial-to-aortic bypass. Effects of pumping rate on cardiac workload and myocardial oxygen consumption.

The purpose of this study was to analyze left ventricular energetics during asynchronous, pulsatile left atrial to aortic bypass in the failing heart with the use of the pressure-volume relationship. In 12 anesthetized Holstein calves (body weight 94 +/- 7 kg), 10 microns microspheres (3.3 x 10(7) +/- 1.1 x 10(7)/100 gm left ventricular weight) were injected into the left main coronary artery to induce heart failure. Baseline left ventricular end-systolic elastance significantly decreased from 7.9 +/- 0.7 to 5.5 +/- 0.4 mm Hg/ml 100 gm left ventricular weight. Left ventricular pressure was measured with a micromanometer, and ultrasonic dimension transducers measured left ventricular orthogonal diameters. Ellipsoidal geometry was used to calculate simultaneous left ventricular volume. End-systolic elastance, pressure-volume area, external work, potential energy, and myocardial oxygen consumption were analyzed during steady-state contractions. After pre-pulsatile left atrial to aortic bypass measurements were taken, the measurements were repeated during asynchronous pulsatile left atrial to aortic bypass at the maximal pumping rate (69 +/- 13 beats/min) termed 100%, and then 80%, 60%, and 40% of the maximal pumping rate in the full to empty mode. With increases in pumping rate, pressure-volume area and external work proportionally decreased, whereas potential energy remained unchanged except for 100% of maximal pumping rate. Pressure-volume area correlated linearly with myocardial oxygen consumption during asynchronous pulsatile left atrial to aortic bypass (r = 0.971). As a result, pumping rate correlated linearly with conservation of myocardial oxygen consumption (r = 0.998). In conclusion, decreased pressure-volume area accounts for the reduction in myocardial oxygen consumption during asynchronous pulsatile left atrial to aortic bypass. Conservation of myocardial oxygen consumption is mainly attributed to the reduction of external work.

Animals↗

PubMed1995

Linear end-systolic pressure-volume relationship during pulsatile left ventricular bypass represents native heart function.

This study assessed whether the end-systolic pressure-volume relationship obtained without any interventions during pulsatile left ventricular bypass adequately represents native heart function. In 11 anesthetized Holstein calves, left ventricular pressure was measured with a micromanometer while left ventricular volume was simultaneously calculated from orthogonal left ventricular diameters measured with ultrasonic dimension transducers. End-systolic pressure and volume data were subjected to linear regression analysis to achieve an end-systolic pressure-volume relationship. Data from both caval occlusions and aortic occlusion were used for the control end-systolic pressure-volume relationship (median r = 0.941, slope = 7.4 +/- 0.8 mm Hg per milliliter per 100 gm left ventricular weight; mean +/- standard error of the mean). During left atrial-aortic bypass with a Pierce-Donachy pneumatic assist pump in the asynchronous mode, the end-systolic pressure-volume relationships were obtained without interventions to change ventricular loading conditions. During maximal ventricular unloading during full to empty pumping, termed 100%, the resulting narrow range of pressure and volume data did not yield highly linear end-systolic pressure-volume relationships (median r = 0.669, slope = 4.9 +/- 0.9 mm Hg per milliliter per 100 gm left ventricular weight). However, at reduced rates off pumping, the end-systolic pressure-volume relationships were considerably linear (80%, median r = 0.819; 60%, median r = 0.868; 40%, median r = 0.899). Slopes did not significantly differ from control values (80%, 6.9 +/- 1.1; 60%, 8.2 +/- 1.1; 40%, 7.8 +/- 1.1). The end-systolic pressure-volume relationship obtained without exogenous load changes during asynchronous, pulsatile left ventricular bypass represents native left ventricular systolic function.

Animals↗

PubMed1995

Explorations into development of a neurally regulated cardiac pacemaker.

Although the artificial cardiac pacemaker has contributed to the management of patients with serious arrhythmias, its rate-responsive function is not sufficient to provide physiological regulation of heart rate (HR). To achieve truly physiological rate response in any given patient, we propose a framework to develop a pacemaker directly regulated by sympathetic nerve activity (SNA). In eight anesthetized rabbits, we quantified the dynamic transduction characteristics from SNA to HR as a transfer function. We then characterized the decoding rule as an impulse response, that is the transfer characteristics in the time domain. The transfer function was approximated by a first-order, low-pass filter with lag time (corner frequency: 0.024 +/- 0.013 Hz, lag time: 0.98 +/- 0.09 s). Predicted HR correlated well with measured HR (r = 0.80-0.98). The standard error of the prediction relative to mean HR was only 1.2 +/- 0.7%, indicating that the prediction was reasonably accurate. Direct decoding of SNA to predict instantaneous HR is possible through this analysis. This framework should enable development of a neurally regulated artificial pacemaker.

Animals↗

PubMed1995

Evaluation of bi-level image converting methods for nuclear medicine image database stored in the IS&C magneto-optical disk.

1. INTRODUCTION. We have developed a report and imaging management system for nuclear medicine. The report and image data are stored in the IS&C magneto-optical disk (IS&C MOD). Nuclear medicine image data are relatively small, but they are large enough to create problems when being transported over a low-speed Hospital Information System (HIS) network. Moreover, gray scale image output devices (i.e., high-resolution displays, sonoprinters) are expensive. If high quality bi-level (black and white) images were available, images could be transferred through low-speed network with inexpensive bi-level terminals or conventional page-printers. We examined images using several bi-level image conversion techniques [1, 2] in order to determine how useful the bi-level images are and to assess their suitability for use in nuclear medicine. The images were compared with original film images by ROC analysis. The modified minimized average error method was found to be superior to other methods in bone and gallium images. Its A-values are 0.83 in gallium scan and 0.85 in bone scan. 2. MATERIALS AND METHODS. Our system consists of three digital gamma cameras, a nuclear medicine data processing unit, two UNIX stations, and two personal computers. The computers and the data processing unit are connected via Ethernet and each computer has an IS&C MOD unit. Image and report data are stored in the IS&C MOD. The computers are also connected off-line through the IS&C MOD. To evaluate image quality, bone scan images and gallium scan images (1024x512, 2048x1024 pixels and 16 bits depth) were converted to bi-level images (same pixels and one bit depth) using four methods: dither method, minimized average error method (MAE)[1], modified regional adaptation method, and constrained average method. For the dither methods, three sets of dither matrix (Fatting's, Bayer's and our original matrix) were employed. The computer images were compared with original film images by ROC analysis. 3. RESULTS. The converted bi-level images were 1/16 the size of the originals. They were transferred via Ethernet, displayed on the monochrome display, and printed using a conventional page-printer (240 dpi or 300 dpi). The A-values of the original gallium and bone images on the films were 0.89 and 0.94. Modified MAE method gave better results than other methods tested, with the gallium image using this technique reading 0.83 on the A-scale; and the bone images were 0.85. 4. DISCUSSION. Generally, nuclear medicine images require lower spatial and gray level resolution than other computer imaging techniques. We compared four bi-level image conversion methods in order to know which methods are suitable to nuclear medicine images. The ROC analysis was employed to evaluate these image qualities. The MAE methods made particular texture pattern as artifacts in the intermediate gray level area. But it can express homogeneity the neutral level. The dither method images are coarse texture. It affects detectabilities of subtle abnormal findings. 5. CONCLUSIONS. The A-z values of the modified MAE images were comparable to those of original film images. Although bone images give slightly lower values, many abnormal findings can be ascertained on bi-level images. High quality bi-level image techniques are considered to be useful for nuclear medicine image database systems.

Japan↗

PubMed1995

Development of a personal computer's viewing station for the IS&C magneto-optical disk.

We developed a display station for the medical images stored in the IS&C (Image Save and Carry) magneto-optical disk. This station consisted of the personal computer and the magneto-optical disk drive. The performance of this system was evaluated and was compared with the Unix workstations. We found that the personal computer system had an adequate ability to display medical images. It provided, moreover, for portability and practical use of medical information.

Data Display↗

PubMed1994

Hypercapnic acidosis increases oxygen cost of contractility in the dog left ventricle.

The effect of acidosis on left ventricular (LV) mechanoenergetics was assessed in seven excised, cross-circulated dog hearts with the use of the frameworks of the contractility index (Emax) and the relationship between myocardial oxygen consumption (VO2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO2 and air in a membrane oxygenator in the coronary arterial perfusion circuit. Acidosis [pH: 6.98 +/- 0.09 (SD), PCO2: 91 +/- 25 mmHg in the coronary arterial blood] decreased Emax by 45 +/- 12% (P < 0.01) and PVA by 47 +/- 12% (P < 0.01) at a fixed LV volume. When the preacidosis Emax level was restored by Ca2+ infusion during acidosis, unloaded VO2 (the VO2 intercept of the VO2-PVA relation) exceeded the control value by 19 +/- 17% (P < 0.05), indicating that acidosis required higher VO2 for nonmechanical activities at a matched Emax. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded VO2 to Emax) was 1.53 +/- 0.40 times higher (P < 0.01) during acidosis than preacidosis. We conclude that acidosis results in LV contractile dysfunction accompanied by an increased oxygen cost of contractility. This increased energy cost of the excitation-contraction coupling can be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.

Acidosis↗

PubMed1994

The effects of dynamic cardiac compression on ventricular mechanics and energetics. Role of ventricular size and contractility.

The purpose of this study was to determine the role of ventricular size or contractility in the effectiveness of dynamic cardiac compression in terms of the pressure-volume relationship and myocardial oxygen consumption. In 10 isolated cross-circulated dog hearts, the ventricle was directly compressed during systole. For the volume run, measurements for slope of the end-systolic pressure-volume relation, pressure-volume area, external work, coronary blood flow, and myocardial oxygen consumption were achieved before and during a fixed amount of dynamic cardiac compression. Left ventricular volume was then increased while stroke volume was kept constant, and measurements were repeated. For the contractility run, after the control measurements were taken, left ventricular contractility was significantly increased or decreased by infusion of either dobutamine or propranolol into the coronary circulation. Measurements were repeated before and during dynamic cardiac compression at the control level of end-diastolic and stroke volumes. Dynamic cardiac compression significantly increased slope of the end-systolic pressure-volume relation, pressure-volume area, and external work (p < 0.01), whereas coronary blood flow and myocardial oxygen consumption were not affected. The increase in pressure-volume area caused by dynamic cardiac compression was greater with the larger volume. Despite the significant differences in the native left ventricular contractility, the increases in slope of the end-systolic pressure-volume relation, pressure-volume area, and external work did not differ among the three groups. We conclude that dynamic cardiac compression enhances left ventricular systolic function independent of ventricular contractility and without affecting coronary blood flow or myocardial oxygen consumption. Mechanical enhancement is more effective in the dilated heart.

Animals↗

PubMed1994

Left ventricular mechanics during synchronous left atrial-aortic bypass.

The purpose of this study was to analyze left ventricular mechanics during asynchronous, pulsatile left atrial-aortic bypass before and after microsphere injection with the pressure-volume relationship. In 14 anesthetized Holstein calves, left ventricular pressure was measured with a micromanometer and ultrasonic dimension transducers measured left ventricular orthogonal diameters. Ellipsoidal geometry was used to calculate simultaneous left ventricular volume. Contractility index, pressure-volume area, external work, and potential energy were calculated during steady-state contractions. These measurements were repeated during pulsatile left atrial-aortic bypass. To induce heart failure, we injected microspheres into the left main coronary artery, and the protocol for baseline and pulsatile left atrial-aortic bypass was repeated. Despite the significant differences in the baseline contractility index (7.4 +/- 0.7 mm Hg/ml versus 4.7 +/- 0.5 mm Hg/ml), contractility index remained the same during pulsatile left atrial-aortic bypass in control and heart failure modes, respectively. Pulsatile left atrial-aortic bypass significantly decreased end-diastolic volume (22% and 17%), pressure-volume area (58% and 48%) and external work (74% and 69%, all p < 0.05) during control and heart failure measurements, respectively. However, it did not change end-systolic volume or potential energy. In conclusion, asynchronous pulsatile left atrial-aortic bypass did not affect left ventricular contractile state in either the normal or failing heart. Although decreased pressure-volume area accounts for the reduction in myocardial oxygen consumption, unchanged potential energy suggested a limited unloading of the ventricle.

Animals↗

PubMed1993

Coupling between regional myocardial oxygen consumption and contraction under altered preload and afterload.

OBJECTIVES: This study was designed to assess the relation between left ventricular regional myocardial oxygen consumption (VO2) and variables of regional myocardial contractile function under various loading conditions. BACKGROUND: Although the relation between global VO2 and global ventricular function has been extensively studied, the relation between regional VO2 and regional myocardial contraction is not fully understood. METHODS: Myocardial shortening (regional area shrinkage), regional work, regional total mechanical energy index and regional VO2 were measured under variously altered loading conditions in the isolated, blood-perfused dog left ventricle. Regional total mechanical energy per beat was quantified by wall tension-regional area area (TAA) by the analogy of left ventricular pressure-volume area. Left ventricular loading conditions were altered by changing end-diastolic volume and stroke volume with a servo pump as follows: 1) increased preload (increased end-diastolic volume and stroke volume at a constant ejection fraction), 2) decreased afterload (increased stroke volume at a constant end-diastolic volume), 3) increased preload and afterload (increased end-diastolic volume at a constant stroke volume), and 4) altered mode of contraction (ejecting vs. isovolumetric contractions). RESULTS: During increased preload, all three variables correlated positively with regional VO2 (r = 0.78 to 1.00). During decreased afterload, the correlation was negative for area shrinkage (r = -0.65 to -0.91) and variable for regional work (r = -0.55 to 0.98) but positive and highly linear for TAA (r = 0.80 to 0.99). During increased preload and afterload, the correlation was again negative for area shrinkage (r = -0.77 to -0.97) but positive for regional work (r = 0.83 to 0.93) and TAA (r = 0.95 to 0.99). During altered mode of contraction, the correlation was insignificant for area shrinkage (r = 0.24 to 0.57) and moderate for regional work (r = 0.50 to 0.79), whereas again highly linear for TAA (r = 0.95 to 0.98). Thus, only TAA correlated closely with regional VO2 under any loading conditions. Furthermore, the slope and regional VO2 intercept of the regional VO2-TAA relation was remarkably consistent among the different hearts and loading conditions. CONCLUSIONS: We conclude that there is a tight coupling between regional VO2 and regional total mechanical energy represented by TAA regardless of left ventricular afterload and preload conditions.

Animals↗

PubMed1993

Ejecting deactivation does not affect O2 consumption-pressure-volume area relation in dog hearts.

We studied the effects of ejection velocity and resistive properties of the left ventricle (LV) on myocardial oxygen consumption (VO2) in 13 excised cross-circulated dog hearts. Increases in peak ejection velocity (-dV/dt) from 4.0 +/- 1.3 (SD) end-diastolic volume (EDV)/s to 12.7 +/- 5.3 EDV/s with constant EDV and end-systolic volume (velocity run) induced systolic pressure deficit. This decreased pressure-volume area (PVA; a measure of ventricular mechanical energy) and LV end-systolic elastance (Emax) by 47 +/- 14 and 38 +/- 15%, respectively. Unchanged maximum rate of left ventricular pressure rise and time-varying elastance during the isovolumic contraction period at the same EDV indicated that these contractions started with the same contractile state although the quicker ejection caused the greater deactivation. If the PVA deficit due to systolic pressure deficit is attributable to an internal energy-dissipating resistive element, VO2 in the velocity run will not as much decrease in proportion to PVA as in the isovolumic or slowly ejecting control run. However, the decreases in PVA due to increased -dV/dt decreased VO2 to the same extent as in the control run. This result negated the possibility that the pressure and PVA deficits would be caused by a mechanical energy-losing process. The same results were obtained whether or not Emax was decreased by quick ejection. We conclude that the pressure and PVA deficits and the proportionally decreased VO2 during quick ejection are mainly attributable to suppression of a ventricular mechanical energy generation process, but not of mechanical energy-losing process, by ejecting deactivation.

Animals↗

PubMed1993

Ryanodine wastes oxygen consumption for Ca2+ handling in the dog heart. A new pathological heart model.

Ryanodine (RYA) at a low concentration (several tens of nM) is known to selectively bind to Ca2+ release channels in sarcoplasmic reticulum (SR) and to fix them open. The present study was designed to investigate the effects of the selective change in Ca2+ release channel activity on cardiac mechanoenergetics as a model of Ca(2+)-leaky SR observed in pathological hearts. We analyzed the negative inotropic effect of RYA at a low concentration (up to 30 +/- 13 nM) on left ventricular (LV) mechanoenergetics using frameworks of LV Emax (a contractility index) and the myocardial oxygen consumption (LV VO2)-systolic pressure-volume area (PVA) (a measure of total mechanical energy) relation in 11 isolated, blood-perfused dog hearts. RYA significantly decreased Emax by 42%, whereas PVA-independent VO2 remained disproportionately high (93% of control). This oxygen-wasting effect of RYA was quite different from ordinary inotropic drugs, which alter Emax and PVA-independent VO2 proportionally. The present result suggests that RYA suppresses force generation of cardiac muscle for a given amount of total sequestered Ca2+ by SR in a similar way to myocardial ischemia and stunning. We speculate about the underlying mechanism that RYA makes SR leaky for Ca2+ and thereby wastes energy for Ca2+ handling by SR.

Analysis of Variance↗

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↗