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H Suga

Publications and source records attributed to H Suga.

At least 271 records · Page 15Linked to original sources
PubMed1984

Energetics of ventricular contraction as traced in the pressure-volume diagram.

The pressure-volume (P-V) relationship of the canine left ventricle can reasonably be simulated by a time-varying elastance model. In this model the total mechanical energy generated by a contraction can be determined theoretically from the change in the elastance. Applying this theory to the actual left ventricle, we have found that the area in the P-V diagram circumscribed by the end-systolic P-V relation line, the end-diastolic P-V relation curve, and the systolic segment of the P-V trajectory is equivalent to the total mechanical energy generated by ventricular contraction. We call this area the systolic P-V area (PVA). We have studied experimentally the correlation between the PVA and myocardial oxygen consumption (VO2) in the canine left ventricle. VO2 was linearly correlated with PVA regardless of the contraction mode and loading conditions in a given left ventricle. The VO2-PVA relation parallel shifted upward with positive inotropic agents. This shift comprised a significant increase in VO2 component for the unloaded contraction. We therefore consider that further analyses of the VO2-PVA relationship will greatly promote our understanding of cardiac energetics.

Animals↗
PubMed1983

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

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.

Animals↗
PubMed1983

Effect of positive inotropic agents on the relation between oxygen consumption and systolic pressure volume area in canine left ventricle.

We analyzed the effect of positive inotropic agents on the relation between left ventricular oxygen consumption and the systolic pressure-volume area. Pressure-volume area is a measure of total mechanical energy for ventricular contraction, and is a specific area in the ventricular pressure-volume diagram circumscribed by the end-systolic and end-diastolic pressure-volume relation curves and the systolic segment of the pressure-volume trajectory. Either epinephrine (1 microgram/kg per min, iv) or calcium ion (0.03 mEq/kg per min, iv) was administered to canine excised cross-circulated hearts. These agents increased an index of ventricular contractility, Emax, or the slope of the end-systolic pressure-volume line, by 70%. The regression lines of ventricular oxygen consumption on pressure-volume area in control and in enhanced contractile states were of the same formula: ventricular oxygen consumption (ml O2/beat per 100 g) equals A times pressure-volume area (mm Hg ml/beat per 100 g) plus a constant B. Coefficient A remained unchanged at 1.8 X 10(-5) ml oxygen/(mm Hg ml), but constant B increased from 0.03 ml oxygen/beat per 100 g by more than 50% with either agent. The reciprocal of A reflects the energy conversion efficiency for the total mechanical energy, and this efficiency remained near 36%. The increase in B was equal to the directly measured increment in ventricular oxygen consumption for mechanically unloaded contraction. The basal metabolism remained unchanged. We conclude that the augmented oxygen consumption under the acutely enhanced contractile state with either epinephrine or calcium was caused primarily by an increased energy utilization associated with the excitation-contraction coupling.

Animals↗
PubMed1982

Mechanism of higher oxygen consumption rate: pressure-loaded vs. volume-loaded heart.

The greater cardiac oxygen consumption (VO2) under pressure than under volume load has been accounted for by the greater ventricular wall force under pressure load. We cannot fully agree with this because the wall force has not always been uniquely correlated with VO2. We attempted to account for the greater VO2 under pressure load by the ventricular systolic pressure-volume area (PVA), which we previously showed uniquely correlated with VO2. In isolated supported canine hearts, we produced servo-controlled ejecting contractions the stroke work (SW) of which was doubled from control by doubling ejection pressure (P) with comparable stroke volume (SV) and by doubling Sv with comparable P. Despite comparable increments in SW from 370 to 680 mmHg.ml under two different loads, VO2 and PVA increased significantly more under pressure load (from 0.033 ml O2/beat and 800 mmHg.ml to 0.0560 and 1,800, respectively) than under volume load (increasing to 0.038 and 1,200, respectively; P less than 0.01). These results suggested to us a new mechanism underlying the greater VO2 under pressure load.

Animals↗
PubMed1982

Factors delaying end ejection from end systole of ventricle.

Although the end of ejection of the left ventricle has been generally accepted as almost synonymous with the end of mechanical systole of the ventricle, recent experimental studies showed the cases in which end ejection lagged markedly behind end systole as identified by the time at which the ventricular pressure-volume data point reached the peak isovolumic pressure-volume relation curve. To obtain a better insight into cardiovascular conditions of the delayed end ejection, a computer simulation study was carried out in which the performance of a time-varying elastance model of the ventricle connected with a modified Windkessel model of the arterial load was analyzed. Any change in the Windkessel parameters, ventricular contractility and heart rate sensitively shifted end ejection relative to end systole. Although end ejection coincided with end systole under limited circumstances, end ejection variably lagged behind end systole undermost circumstances. These results suggest that the interval between end systole and end ejection of the left ventricle in vivo is also variable depending on changes in the arterial loading conditions, ventricular contractility and heart rate.

Cardiac Output↗
PubMed1982

Digital on-line computation of a predictor of cardiac oxygen consumption. Left ventricular systolic pressure volume area.

Left ventricular systolic pressure volume area (PVA) has been proposed as a reliable predictor of cardiac oxygen consumption per beat (VO2). PVA is the area in the pressure-volume (P-V) diagram that is circumscribed by the end-systolic and end-diastolic P-V relation curves and the systolic segment of the P-V loop trajectory. It represents the total mechanical energy required for the ventricle to contract, to change its wall's elastic state from end diastole to end systole, and to eject blood against afterload. PVA has so far been measured manually with a planimeter applied to the P-V diagram. To measure PVA more accurately and on line during experiments, we devised a new method of computing PVA with a digital computer. The method consists of integrating during systole the infinitesimally narrow triangular pressure volume area swept by the straight line segment connecting Vd (ventricular volume at which peak isovolumic pressure is zero) and the instantaneously counterclockwise moving P-V data point in the P-V plane, and adding a small area between the end-diastolic P-V relation curve and the line connecting Vd and the end-diastolic P-V point. This method has proved useful in our study of the relation between VO2 and PVA to evaluate the PVA's ability to predict VO2.

Blood Pressure↗
PubMed1981

Calorimetric studies of adenosine 5'-triphosphate hydrolysis by heavy meromyosin.

The heat production for the reaction steps of ATP hydrolysis by heavy meromyosin has been reexamined by using a reaction-type calorimeter. So far, the values reported for the heat production have varied substantially among research groups. The present results obtained in 0.3 M KCl, 10 mM MgCl2, and 20 mM Tris-HCl at pH 8.0 and 20 degrees C show that (1) the binding and splitting of ATP on the myosin head are moderately exothermic (delta H = -23 kJ mol-1), (2) the decomposition of the M.ADP.Pi intermediate complex to M.ADP + Pi is strongly exothermic (delta H = -66 kJ mol-1), and (3) the dissociation of ADP from the myosin head is strongly endothermic (delta H = +60 kJ mol-1). These results agree with our previous findings that the decomposition of M.ADP.Pi as well as the binding of ADP to heavy meromyosin is strongly exothermic [Yamada, T., Shimizu, H., & Suga, H. (1973) Bio-chim. Biophys, Acta 305, 642-653].

Adenosine Diphosphate↗
PubMed1981

Ventricular systolic pressure-volume area as predictor of cardiac oxygen consumption.

We scrutinized the recently reported correlation between the canine left ventricular systolic pressure-volume area (PVA) and cardiac oxygen consumption rate per beat (Vo2) by use of an improved method of Vo2 assessment. PVA is the specific area in the pressure-volume (PV) plane bounded by the end-systolic and end-diastolic PV lines and the systolic segment of the PV loop. Different from the previous study in which Vo2-PVA data from isovolumic and ejecting contractions were pooled for analyses, we analyzed Vo2-PVA data from the two different modes separately to examine whether there was any difference of Vo2-PVA relationship between them. The results indicated that the linear regressions of Vo2 on PVA were virtually the same for isovolumic and ejecting contractions. The regression line was Vo2 (ml O2/beat) = a[PVA (mmHg x ml x beat-1)] + b, where a = 1.64 (+/- 0.12 SE) X 10(-5) (ml O2/beat)/(mmHg x ml x beat-1) and b = 0.015 +/- 0.002 ml O2/beat in 10 hearts. We conclude that PVA serves as a reliable predictor of Vo2 regardless of the mode of contraction in a given left ventricle with a stable inotropic background.

Animals↗
PubMed1981

Regression of cardiac oxygen consumption on ventricular pressure-volume area in dog.

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 is the specific area in the pressure-volume (PV) diagram, consisting of the area (EW) within the PV loop and the area (PE) bound by the end-systolic and end-diastolic PV lines and the relaxation segment of the PV loop. EW and PE correspond to the external mechanical work and the end-systolic elastic potential energy in the ventricular wall, respectively. We determined the optimal combination of EW and PE for the best prediction of VO2, using the linear multiple regression analysis. From EW, PE, and VO2, data of many isovolumic and ejecting contractions, the optimal coefficients of EW and PE were 1.67 +/- 0.43 (SD; 7 hearts) and 1.74 +/- 0.49 (10(-5) ml O2/mmHg . ml), virtually identical to each other, corroborating that PVA, i.e., a simple sum of EW and PE, can reliably predict VO2 of a given heart in a stable contractile state.

Animals↗
PubMed1981

Equal oxygen consumption rates of isovolumic and ejecting contractions with equal systolic pressure-volume areas in canine left ventricle.

Left ventricle systolic pressure-volume area (PVA) has been found to be highly linearly correlated with cardiac oxygen consumption rate per beat (VO2) in a given canine heart with a stable inotropic background. PVA is a specific area in the pressure-volume (P-V) diagram that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop, consisting of the sum of external mechanical work and what is considered the end-systolic elastic potential energy in the ventricular wall. In this study, we compared VO2's of steady state entirely isovolumic and variously ejecting contractions that were made to have equal PVA's in the canine left ventricle. We found that VO2's of these isovolumic and ejecting contractions with equal PVA's (isovolumic vs. ejecting = 1008 +/- 64 (SE) vs. 1022 +/- 62 mm Hg ml/beat, n = 32 pairs in 10 hearts) were equal to each other (0.0375 +/- 0.0021 vs. 0.0368 +/- 0.0021 ml O2/beat) regardless of the marked differences in stroke volume (0 vs. 9.8 +/- 0.6 ml), end-diastolic volume (20.3 +/- 0.8 vs. 23.7 +/- 0.9 ml), end-systolic volume (20.3 +/- 0.8 vs. 13.9 +/- 0.7 ml), peak pressure (123 +/- 5 vs. 88 +/- 5 mm Hg), stroke work (0 vs. 636 +/- 36 mm Hg ml/beat), and calculated peak total wall force (1588 +/- 77 vs. 1077 +/- 72 g). Therefore, we conclude that PVA can serve as a reliable predictor of VO2 in a given canine left ventricle with a stable inotropic background whether the contraction mode is isovolumic or ejecting.

Animals↗