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Biomedical subjects

H Suga

Publications and source records attributed to H Suga.

At least 289 records · Page 16Linked to original sources
PubMed1981

Dissociation of end ejection from end systole of ventricle.

Previous experiments showed the cases in which end ejection of the ventricle did not always coincide with end systole as identified by the time for Emax corresponding to the maximally contracted pressure-volume relationship line of the ventricle. The purpose of the present study is to obtain a better insight into the ventricular afterloading conditions that enable end ejection to coincide with end systole of the ventricle by a simulation method. The left ventricle was simulated by a time-varying elastance, E(t), and the afterload by a constant pressure connected to the ventricle via a valve with resistance R and inertance L in series. A sinusoidal wave starting from 0 at onset of systole, reaching Emax at end systole, and returning to 0 at end diastole in each cycle was assigned for E(t). Parameters of the system elements were changed individually. Ventricular pressure, volume and flow were computed by solving the system of ordinary differential equations with a time-varying parameter, E(t). Results indicate that end ejection coincides with end systole only when R and L values fall on a specific curve in an R-L domain for a given set of the other system parameters, and otherwise the 2 ends variably dissociate from each other. Consequently, end ejection should not blindly be used as a substitute for end systole when Emax and end-systolic pressure-volume relations are to be assessed.

Humans↗
PubMed1981

Principle of normal heart adaptation in size and weight to pressure and volume loads.

A hypothesis was proposed for a fundamental principle of adaptation of normal hearts to pressure and volume loads: The end-systolic active stress (P) and shortening fraction (S) of myocardium in the ventricular wall were hypothesized to be preserved near normal levels by the adaptation regardless of heart size and animal species F and S were mathematically related to ventricular wall volume (M) and end-diastolic chamber volume (D) both normalized to stroke volume with afterload pressure (P) as a parameter. The deduced M-P and D-P relationships were compared with corresponding data documented in literature. The actual data from normal hearts including pressure and volume overloaded but compensated hearts of different animal species from rats to horses including human children and adults distributed near the theoretical curves for S=0.1-0.2 and F=60-160 Gm/cm2 despite the 2X10(3) times difference in heart size and weight. However, data from failing and abnormal hearts significantly deviated from those curves. These results seem to support the present hypothesis as a fundamental principle of the adaptation of normal hearts to loads.

Adaptation, Physiological↗
PubMed1981

Alterations of circulatory responses to upright tilt in cardiac patients.

Circulatory responses to the upright tilt were studied in 20 normal subjects and 27 cardiac patients with ischemic heart disease or idiopathic cardiomyopathy. In normal subjects, the upright tilt caused obvious increases in heart rate and diastolic pressure, a slight decrease in systolic pressure and marked decreases in cardiac output and stroke volume. The circulatory changes during the tilt were less pronounced in the cardiac patients as compared with the normal subjects. The reductions of cardiac output and stroke volume and the increase in total peripheral resistance were all significantly diminished. A paradoxical increase in cardiac output during the tilt, an observation hitherto not well recognized, was observed in 5 cases with low cardiac index during the control period. Although several possibilities can be considered for the explanation of the diminished, sometimes paradoxical, circulatory responses to the tilt in cardiac patients, the improvement of the function of the diseased heart by preload reduction was proposed as an important factor. There was a significant negative correlation between the per cent changes of cardiac output and the per cent changes of PEP/LVET. It was suggested that the measurements of systolic time intervals during the tilt might be useful for evaluating the severity of the hemodynamic derangement in cardiac patients.

Adolescent↗
PubMed1981

Real time analog computation of left ventricular systolic pressure volume area as predictor of oxygen consumption.

An analog circuit was devised for real time determination of the left ventricular systolic pressure volume area (PVA), which we had recently identified as a reliable predictor of cardiac oxygen consumption rate per beat. PVA is the specific area in the pressure-volume diagram that is bounded by the end-systolic and end-diastolic pressure-volume relationship lines and the systolic segment of the pressure-volume loop trajectory of the left ventricle. The computed PVA was compared with PVA obtained as usual by planimetry. Correlation coefficient between the two PVA's was 0.997 (N=31, P less than 0.001) and the standard error of mean of the difference between th two PVA's was as small as practically negligible 8 mmHg ml in the PVA range from 0 to 2,000 mmHg ml. We concluded that this PVA analog computer can be used for real time determination of PVA, expediting the future studies of the relationship between PVA and cardiac oxygen consumption.

Animals↗
PubMed1980

Systolic quick releases of nonexcised blood-perfused canine papillary muscle.

Systolic stiffness was studied in five coronary perfused twitching papillary muscles of canine right ventricles. The muscles beat at regular sinus rhythms at 37 degrees C. They were shortened quickly at about 10 muscle lengths/s in the middle of isometric contractions. Systolic force decreased exponentially with the shortening in the force-length diagram. Relating Lagrangian stress (sigma) and strain change (delta epsilon) relative to isometric length calculated from the force-length relationship curve during quick release, I found a linear relationship between ln sigma and delta epsilon. This indicates that the systolic stres-strain relationship of the canine papillary muscle can be approximated by an exponential curve, sigma = sigma m exp(k . delta epsilon), where sigma m = isometric stress at the onset of quick release. The mean +/- SE of the stiffness constant k was calculated to be 55 +/- 8 (dimensionless). These k values are greater than those of excised cat papillary muscles at 37 degrees C reported in literature. This difference in k values may be ascribed to the difference in the mechanical property of the uncut pinned end of the present preparation as opposed to the cut clamped end of the conventional preparation, although the canine and feline papillary muscles may simply have the different k values.

Animals↗
PubMed1980

Transient tension responses of heart muscle in Ba2+ contracture to step length changes.

To characterize mechanical properties of activated heart muscle, kitten papillary muscles in Ba2+ contracture were stretched or released stepwise, and the transient tension responses were analyzed. Various amplitudes of step length change (0.1-1.0% of Lmax) were tested from different initial lengths and at different temperatures. The tension response to either stretch or release showed four different phases, which were nearly symmetric when the input length change was 0.1% of Lmax. When the length changes was 1%, the second phase of stretch response became shorter, whereas that of release became longer. The third phase of stretch response was prolonged, whereas that of release response became obscure. The peak tension (F1) in the first phase was linearly related to the amplitude, whereas those in the second and third phase were not. Increasing temperature markedly decreased F1 and shortened the second and third phase independently of initial muscle length. These results were consistent with those properties of heart muscle in Ba2+ contracture previously characterized with sinusoidal length changes.

Animals↗
PubMed1980

Critical evaluation of left ventricular systolic pressure volume areas as predictor of oxygen consumption rate.

Left ventricular systolic pressure volume area (PVA) has been reported to be a reliable predictor of cardiac oxygen consumption rate per beat (VO2) in a given heart with a stable inotropic background. PVA has been defined as the specific area in the pressure-volume (P-V) plane that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop trajectory. In the present experimental study, we separated PVA into two parts: EW and PE. EW is the area surrounded by the P=V loop, corresponding to the external mechanical work. PE is the area surrounded by the end-systolic and end-diastolic P-V lines and the relaxation segment of the P-V loop, corresponding to what is considered the end-systolic elastic potential energy in terms of a time-varying elastance model of the ventricle. We attempted to find an optimal weighting coefficient K of PE for the best correlation between VO2 and PVAW = EW + K . PE, changing K from 0 to infinity. Results in 7 canine excised cross-circulated hearts showed that PVAW best correlated with VO2 at K = 1.03 +/- 0.03 (SE). Since PVAW at K = 1 is identical with the original PVA, we concluded that PVA could serve as a reliable predictor of VO2. PVA is concluded to be physiologically significant in the coupling between cardiac mechanics and energetics.

Animals↗
PubMed1979

External mechanical work from relaxing ventricle.

The possibility has been proposed earlier that the specific pressure-volume (P-V) area bounded by the left ventricular end-systolic and end-diastolic P-V curves and the isovolumic relaxation part of the P-V loop represents mechanical potential energy that has been built during systole and is stored at end systole in the wall of the ventricle. In the present study on canine left ventricles, as much as 70% of the P-V area was actually converted into external mechanical work when ventricular volume was allowed to decrease at an appropriate speed (about 55 ml/s in 70 g left ventricle) during relaxation. Less external work was extracted from the same P-V area when the speed of volume reduction was either higher or lower than that speed. These results indicate that the P-V area is equivalent to a form of potential energy, which is wasted with isovolumic relaxation but most of which is convertible to external mechanical work if the ventricle is allowed to eject against an appropriately decreasing afterload during relaxation.

Animals↗
PubMed1979

Total mechanical energy of a ventricle model and cardiac oxygen consumption.

Mechanical energy (ENG) required by a time-varying elastance model of the ventricle was compared with oxygen consumption per beat (VO2) of the canine left ventricle contracting under a variety of loading conditions. ENG needed for this model to increase its elastance during systole is shown to be equal to the sum of the potential energy built in the elastance during systole plus the external mechanical stroke work. This ENG is equivalent to the area (PVA) bounded by the end-systolic and end-diastolic P-V curves and the systolic limb of the P-V loop trajectory in the P-V plane. There was a high correlation (r = 0.89) between VO2s documented in the literature and PVAs assessed by the author from the accompanying P-V data from both isovolumic and ejecting contractions in 11 hearts. A linear regression analysis yielded an empirical equation: VO2 (ml O2/beat) = a . PVA (mmHg . ml/beat) + b, where a = 1.37 X 10(-5) and b = 0.027, which can be used to predict VO2 from PVA. A preliminary experimental study in my laboratory confirmed the validity of this empirical equation.

Elasticity↗
PubMed1979

Accuracy of ventricular lumen volume measurement by intraventricular balloon method.

To assess the accuracy of left ventricular volume measured by the intraventricular balloon method, we measured the space between the endocardium and the gradually inflated balloon in six Formalin-fixed canine left ventricles. The space was as small as 1-1.5 ml for intraballoon pressure of 100-200 mmHg and tended to increase to 2 ml with decreases in pressure to 50 mmHg.

Animals↗
PubMed1979

Instantaneous pressure-volume relationship of right atrium during isovolumic contraction in canine heart.

We studied the contraction of the right atrium in an excised cross-circulated heart preparation. Atrial volume and instantaneous atrial pressure were measured in a water-filled balloon fitted in the spontaneously contracting right atrium. The relation of instantaneous pressure to volume was analyzed by collecting pressure data from multiple isovolumic contractions with different volumes but measured at multiple identical time points in the contraction cycle. The relation was found to be quasi-linear during most of atrial systole and diastole. A linear regression formula P(t) = K(t)[V- VD(t)] was therefore fitted to the data. K(t) and VD(t) of the regression formula are the slope and the volume axis intercept in the pressure-volume plane, respectively. When the atrium beat spontaneously at a regular sinus rhythm with no inotropic intervention. K(t) increased during systole and decreased during diastole, whereas VD(t) decreased during systole and increased during diastole. The average value of K was 13 +/- 1.7 (SE) mmHg . kg . ml-1 at the end of diastole and 33 +/- 0.02 (SE) mmHg . kg . ml-1 at the end of systole. The average value of VD was 0.303 +/- 0.017 (SE) ml . kg-1 at the end of diastole and 0.212 +/- .025 (SE) ml . kg-1 at the end of systole. Enhancement of contractility with epinephrine or Ca2+ significantly increased the value of K at the end of systole, but it did not significantly affect either K at the end of diastole or VD at the end of systole and diastole.

Animals↗
PubMed1979

Graphical estimation of ventricular wall force and stress from pressure-volume diagram.

A graphical method is proposed for assessment of ventricular wall circumferential total force and mean stress from the ventricular pressure-volume diagram. A family of force or stress isopleths are first drawn in the pressure-volume plane using a geometric model of the left ventricle and an appropriate version of the Laplace equation. A pressure-volume loop of the ventricle to be analyzed is then drawn in this pressure-volume plane. Total circumferential force in the ventricular wall or its mean circumferential stress can now be read directly from the intersections of the pressure-volume loop with the force or stress isopleths.

Cardiac Volume↗
PubMed1979

Left ventricular systolic pressure-volume area correlates with oxygen consumption.

In 13 excised, cross-circulated canine hearts, we studied the correlation between left ventricular oxygen consumption per beat (MVO2) and the magnitude of a specific pressure-volume (P-V) area circumscribed by the end-systolic and end-diastolic P-V relationship curves and the systolic segment of the P-V trajectory of a left ventricular contraction. The pressure and volume load of the ventricle were changed with a volume servo pump in order to alter the P-V area, and MVO2 was measured (after each change in the pressure and volume load). In the data collected from both isovolumic and ejecting contractions of each left ventricle contracting with a stable inotropic background, we found a linear correlation between MVO2 and the P-V area. The average correlation coefficient was 0.92 +/- 0.016 (SE). Linear regression analysis yielded the formula: MVO2 (ml/beat) = alpha[P-V area (mmHg.ml/beat)] + b, where alpha, the slope coefficient, was (1.53 +/- 0.14) x 10(-5) and b, which probably represents the basal O2 consumption, was 0.019 +/- 0.003 ml/beta. We propose that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.

Animals↗