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Biomedical subjects

H Suga

Publications and source records attributed to H Suga.

At least 217 records · Page 12Linked to original sources
PubMed1989

Right ventricular mechanical and energetic properties.

To formulate right ventricular (RV) mechanical and energetic properties in terms of the time-varying elastance model, Emax and the systolic pressure-volume area (PVA) of RV were measured in the excised cross-circulated heart preparation, while the left ventricle was beating unloaded. Emax of RV was constant, and independent of the RV volume, the stroke volume, the ejection velocity, and the pre-ejection period in the control contractile state. Enhancement of the contractile state with calcium increased Emax, and reduction of the contractile state with propranolol decreased Emax. The whole heart oxygen consumption (Vo2) was linearly regressed on PVA of RV, in both the control and the calcium-enhanced contractile state. Calcium elevated the regression line in a parallel manner. The slope of the regression line was (1.85 +/- 0.19) x 10(-5) ml O2/mmHg ml in the control state, and (1.57 +/- 0.44) in the calcium state. These slope values were similar to those in left ventricle (LV). We therefore conclude that mechanical and energetic properties of RV are similar to those of LV.

Animals↗
PubMed1989

[Postoperative pyuria after TUR-P: the study of postoperative pyuria by using NFLX].

The postoperative duration of pyuria was studied in 35 patients who underwent transurethral resection of the prostate (TUR-P). The average postoperative duration of pyuria was 58.0 +/- 23.6 days. The age over 70 years, preoperative indwelling of urethral catheter and the preoperative urinary tract infection did not make the duration of pyuria longer. The volume of resected prostatic tissue over 20 g and the existence of diabetes mellitus make it significantly longer. It is effective and safe to use a low-dose antibacterial agent such as NFLX which has a broad spectrum and hardly develops bacterial resistance after TUR-P. It is suggested unnecessary to change the anti-bacterial agent even when pyuria continues.

Aged↗
PubMed1988

Ventricular systolic pressure-volume area (PVA) and contractile state (Emax) determine myocardial oxygen demand.

We have briefly reviewed the recent advances in the understanding of primary determinants of cardiac oxygen consumption (Vo2). We focused on our own experimental findings that Vo2 is a function of left ventricular systolic pressure-volume area (PVA), as a measure of total mechanical energy generated by contraction, and the left ventricular contractility index (Emax). We conclude that the cardiac oxygen demand of the ongoing contractions is equivalent to Vo2 and is a precise function of PVA and Emax whether coronary oxygen supply is normal or mildly limited in the excised, cross-circulated dog left ventricle. However, when the coronary oxygen supply is severely limited, Vo2 may not always be equivalent to the oxygen demand capability shown by the heart when its coronary oxygen supply is restored.

Animals↗
PubMed1988

The different contributions of coronary blood flow to changes in myocardial oxygen consumption between excised and in situ canine hearts.

The correlations of CBF-MVO2 and AVD-MVO2 were analyzed by linear regression analysis in three groups of canine heart preparations. CBF correlated well with MVO2 in all cases of in situ heart preparations, and the sensitivity of CBF to changes in MVO2 was high. In contrast, AVD, rather than CBF, correlated well with MVO2 in all cases of excised hearts, and the sensitivity of CBF to changes in MVO2 was low. The different manner of oxygen delivery in excised hearts from that in situ hearts can be attributed to the characteristics of its coronary perfusion and the impaired mechanism of metabolic vasoregulation in the coronary vasculature.

Animals↗
PubMed1988

A new cardiotonic agent, OPC-8212, elevates the myocardial oxygen consumption versus pressure-volume area (PVA) relation in a similar manner to catecholamines and calcium in canine hearts.

We studied the effect of a new positive inotropic agent, OPC-8212 (3,4-Dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinolinon e), on the relation between left ventricular oxygen consumption (VO2) and pressure-volume area (PVA) in excised cross-circulated dog hearts. PVA represents the total mechanical energy generated by ventricular contraction. OPC-8212 increased the contractility index, Emax, by 59% +/- 36% from 7.6 +/- 4.3 to 11.1 +/- 4.6 mmHg/(ml/100 g LV [leftventricle]). OPC-8212 elevated the VO2-PVA relation without a significant change in its slope. Namely, OPC-8212 did not affect the mechanical efficiency of the contractile machinery from the PVA-dependent fraction of VO2 to PVA, but increased the PVA-independent fraction of VO2 which is related with non-mechanical processes of contraction. This effect suggested an increased energy expenditure for excitation-contraction coupling. These results associated with the enhanced contractile state by OPC-8212 were both qualitatively and quantitatively similar to those obtained with catecholamines and calcium in our previous study. This suggests that OPC-8212, catecholamines, and calcium have similar effects on intracellular Ca2+ concentration and enhanced ventricular contractility.

Animals↗
PubMed1988

Paired pulse pacing increases cardiac O2 consumption for activation without changing efficiency of contractile machinery in canine left ventricle.

The relation between cardiac O2 consumption (VO2) and the total mechanical energy (TME) generated by contraction was studied under paired-pulse (PP) pacing and compared with that under single-pulse pacing at the same basic rate as PP pacing and at the double-pacing rate in ten excised cross-circulated canine left ventricles (LV). TME was assessed by the systolic pressure-volume (P-V) area (PVA) defined as the area bounded by the end-systolic and end-diastolic P-V curves and the systolic P-V trajectory. The VO2-PVA relation was linear under PP pacing as well as at control and double heart rates. PP pacing increased LV contractility index Emax from 6.3 +/- 3.3 (SD) to 18.0 +/- 8.6 mmHg/(ml/100 g) and elevated markedly the VO2-PVA relation by increasing the VO2-axis intercept (or PVA-independent VO2) from 0.62 +/- 0.11 to 1.13 +/- 0.35 J.beat-1.100 g-1. However, PP pacing did not change the slope of the VO2-PVA relation at 2.24 +/- 0.53 (dimensionless). The efficiency from PVA-dependent VO2 (total VO2-PVA-independent VO2) to PVA (=TME), calculated as the reciprocal of the slope of the VO2-PVA relation, was also constant at 47 +/- 11% regardless of PP pacing. These results are similar to previous results obtained by positive inotropic interventions with catecholamines and Ca2+. We conclude that PP pacing augments the PVA-independent VO2 for activation without affecting the efficiency of the contractile machinery to generate TME from the PVA-dependent VO2.

Animals↗
PubMed1988

Oxygen-saving effect of negative work in dog left ventricle.

We compared left ventricular oxygen consumptions (VO2) of contractions performing negative external work (EW less than 0) and positive external work (EW greater than 0) that developed comparable peak systolic pressures in the excised cross-circulated dog hearts. We changed the polarity of ventricular work with volume servo-pump and measured both left ventricular VO2 and systolic pressure-volume area (PVA). PVA represents the total mechanical energy generated by contraction and is equal to the area circumscribed by the end-systolic and end-diastolic pressure-volume (PV) relation curves and the systolic PV trajectory. For comparable peak systolic pressures of approximately 90 mmHg, contractions performing negative EW of -834 +/- 327 mmHg.ml.100 g left ventricle-1 had 27 +/- 11% smaller VO2 and 62 +/- 12% smaller PVA than those performing positive EW of 851 +/- 329 mmHg.ml.100 g-1. The smaller VO2 for negative EW could be accounted for by the linear VO2-PVA relation regardless of the polarity and magnitude of work. The results indicate that negative work can save VO2 of contractions to develop a given peak systolic pressure.

Animals↗
PubMed1988

O2 consumption of dog heart under decreased coronary perfusion and propranolol.

We compared the effects of decreased coronary perfusion pressure (CP) and propranolol on the relation between left ventricular O2 consumption (VO2) and systolic pressure-volume area (PVA). PVA represents total mechanical energy generated by contraction and is the area under the end-systolic pressure-volume (PV) line and systolic PV trajectory. In excised cross-circulated dog hearts, a decrease in CP from 82 (mean) to 51 mmHg decreased ventricular contractility index Emax (slope of end-systolic PV relation) by 17% (P less than 0.05) and slightly (P less than 0.05 in 3 of 11 hearts) lowered the VO2-PVA relation in a parallel fashion. A further decrease in CP to 32 mmHg decreased Emax by 56% (P less than 0.05) and considerably (P less than 0.05) lowered the VO2-PVA relation by decreasing both the VO2-axis intercept by 26% (P less than 0.05) and the slope by 24% (P less than 0.05) from control. Propranolol decreased Emax by 48% (P less than 0.05) and the VO2-axis intercept by 25% (P less than 0.05) without changing the slope (P greater than 0.05). We attributed the different response of the VO2-PVA relation to the difference of the coronary O2 supply-demand balance between decreased CP and propranolol.

Animals↗
PubMed1988

Integrated regional work equals total left ventricular work in regionally ischemic canine heart.

To assess left ventricular (LV) regional work with physically correct dimensions, wall tension-regional area (T-A) loops were analyzed before and after coronary occlusion in the excised cross-circulated canine LV (n = 11) connected to a volume-servo pump. Wall tension was calculated with the force equilibrium equation for a sphere, and regional areas were determined from pairs of orthogonal sonomicrometers in ischemic and nonischemic regions. LV and regional stroke work were simultaneously assessed from the pressure-volume and T-A loops during one cardiac cycle at various end-diastolic and stroke volumes. After coronary occlusion, regional work of the ischemic region markedly decreased to near or even below zero. Although regional work of the nonischemic region moderately decreased at constant LV end-diastolic and stroke volumes, the contribution of the nonischemic region to LV stroke work increased. Globally integrated regional work calculated from regional work/unit area and estimates of the extent of ischemia closely agreed with measured LV stroke work either before (n = 119; r = 0.92) or after coronary occlusion (n = 141; r = 0.93) despite the marked changes in regional work in both regions. We conclude that the global integral of regional work equals the total LV work and that regional work of the LV can be reliably assessed from the T-A loop with the same dimensions as energy in both normal and regionally ischemic hearts.

Animals↗
PubMed1988

No significant increase in O2 consumption of KCl-arrested dog heart with filling and dobutamine.

In the cross-circulated dog hearts arrested with KCl, we examined the effects of left ventricular volume and dobutamine on the resting oxygen consumption (MVO2). The perfusion pressure of the excised heart was stable under the cross-circulation for 1-1.5 h with a dialyzer to normalize coronary venous KCl despite continuous coronary arterial injection of KCl. The resting MVO2 declined gradually during the first 10 min of cardiac arrest but changed little thereafter. The resting MVO2 at 5 min and 30 min of arrest were 30.5 +/- 9.3 (SD) and 23.8 +/- 12.9%, respectively, of unloaded MVO2 before arrest. The resting MVO2 after its stabilization was 1.02 +/- 0.42 ml O2.min-1.100 g ventricle-1 in the control. It was 1.12 +/- 0.48 ml O2.min-1.100 g ventricle-1 under a continuous infusion of dobutamine at rate of 10-25 micrograms/min. This change with dobutamine was statistically insignificant. The resting MVO2 was not affected by changes in left ventricular volume both before and under dobutamine. The present result implies that MVO2 for basal metabolism in a working dog heart is virtually constant regardless of ventricular volume and contractility.

Animals↗
PubMed1988

Optimal contractility and minimal oxygen consumption for constant external work of heart.

We theoretically considered the relation between left ventricular O2 consumption (MVO2) and a contractility index (Emax), searching for an optimal Emax that minimizes MVO2 for a given external mechanical work. We used one equation relating Emax with ventricular pressure and volume and another equation relating MVO2 with pressure-volume area (PVA). PVA is theoretically and experimentally a good predictor of MVO2 with Emax as a parameter. Then we could theoretically show the existence of the optimal Emax. For example, MVO2 was minimized to 8.9 ml O2.min-1.100 g-1 at an Emax of 6.3 mmHg.ml-1.100 g when cardiac output was 1.2 l/min, afterload pressure was 100 mmHg, and heart rate was 150 beats/min. These values can be observed experimentally in a 10- to 15-kg dog. Optimal Emax values for a wide range of external work fall in the middle of the normal working range of Emax. Thus our MVO2-PVA-Emax relationship supports the contemporary concept of the optimal contractility that MVO2 for a given cardiac external work is minimum at a middle level of ventricular contractility.

Animals↗
PubMed1988

Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

To determine the essential mechanism of increased systolic wall motion, i.e., hyperkinesis, in a nonischemic region (NIR) during acute ischemia, we simultaneously evaluated global and regional function of the excised, cross-circulated canine left ventricle connected to a volume servo pump before and after coronary occlusion. Regional areas were determined with pairs of orthogonal subendocardial sonomicrometers in the ischemic region (IR) and NIR. After coronary occlusion with left ventricular end-diastolic and stroke volumes kept constant, the amount of systolic area shrinkage (delta A) in NIR increased by 33 +/- 41% (p less than .05), despite a decrease in end-diastolic regional area by 3 +/- 4% (p less than .05). Regional work obtained from the wall tension-regional area (T-A) loop in NIR decreased by 50 +/- 24% due to a similar decrease in afterload despite the presence of hyperkinesis, indicating regional systolic unloading. When left ventricular end-diastolic volume was subsequently increased with a constant stroke volume, delta A in NIR increased at the expense of a further decrease in delta A in IR. The end-systolic T-A relationship in NIR remained unchanged, whereas that in IR markedly shifted rightward, suggesting that the contractile state of NIR was constant. These results indicate that hyperkinesis in NIR during acute ischemia can occur without a utilization of the Frank-Starling mechanism or an enhancement of regional contractile state, and that the essential mechanism of this phenomenon is regional afterload reduction due to an intraventricular mechanical interaction between IR and NIR.

Animals↗
PubMed1988

Efficiency of energy transfer from pressure-volume area to external mechanical work increases with contractile state and decreases with afterload in the left ventricle of the anesthetized closed-chest dog.

We studied the effects of ventricular end-systolic elastance (Ees) and effective arterial elastance (Ea) on the efficiency of energy transfer from pressure-volume area (PVA) to external mechanical work (EW) in the left ventricle of anesthetized closed-chest dogs. PVA represents the total mechanical energy generated by ventricular contraction, which is an intermediate form of energy between oxygen consumption, the total energy input, and EW, the effective energy output. PVA and EW were determined from ventricular pressure and volume, which were continuously measured with a volumetric conductance catheter. Measurements of Ees were obtained by transiently increasing afterload by an inflation of a Fogarty catheter in the thoracic descending aorta. Ea was determined as the ratio of end-systolic pressure to stroke volume. The EW/PVA efficiency of a steady-state contraction increased from 55% to 64%, with a 58% increase in Ees after dobutamine. Ees, which was smaller than Ea before dobutamine, became nearly equal to Ea after dobutamine, maximizing EW for a given end-diastolic volume. EW/PVA efficiency decreased with an abrupt increase in afterload before and after dobutamine. The sensitivity of the decrease in the EW/PVA efficiency to an increase in end-systolic pressure was significantly less after than before dobutamine. We could account for all these changes in EW/PVA efficiency by the relative changes in Ees and Ea in the pressure-volume diagram.

Animals↗
PubMed1988

Cardiac cooling increases Emax without affecting relation between O2 consumption and systolic pressure-volume area in dog left ventricle.

We studied the effects of cardiac cooling by 7 +/- 2 degrees C (SD) from 36 degrees C on both contractility index (Emax) and the relation between O2 consumption per beat (VO2) and systolic pressure-volume area (PVA) of the left ventricle in the excised cross-circulated dog heart preparation. PVA represents the total mechanical energy generated by a contraction. The VO2-PVA relation divides measured VO2 into unloaded VO2 and excess VO2. The slope of the VO2-PVA relation represents inversely the efficiency of the contractile machinery to convert chemical energy from the excess VO2 to total mechanical energy. Cooling is known to decrease myosin ATPase activity (Q10 of 2-3), which in turn is expected to increase the chemomechanical efficiency of cross bridges. Therefore, we expected an increase in the efficiency and hence a decreased slope of the VO2-PVA relation with cooling. The cooling increased Emax by 46 +/- 13% and the time to Emax by 45 +/- 27%. Pacing rate was constant or had to be slightly decreased to avoid arrhythmias with cooling. We found that neither the slope of the VO2-PVA relation nor unloaded VO2 significantly (p greater than 0.05) changed with the cooling. This result contradicts the expected increase in the efficiency with cooling. We conclude that cardiac cooling by 7 degrees C from 36 degrees C does not increase the efficiency of the contractile machinery in excised cross-circulated dog left ventricle.

Animals↗
PubMed1988

Pressure-volume relation around zero transmural pressure in excised cross-circulated dog left ventricle.

Left ventricular (LV) pressure-volume (PV) relations of quasi-isobaric contractions around zero transmural pressure were studied with a new volumetric method. Left ventricles of isolated cross-circulated dog hearts were connected to a large air tank through the mitral annulus. The volume of the air space was changed with a volume servo pump to oscillate the transmural pressure (P) around zero. Instantaneous LV volume (V) was computed from P by Boyle's law (P.V = constant) to draw the PV trajectories of the isobaric contractions. The end-systolic PV relation (ESPVR) and end-diastolic PV relation (EDPVR) curves intercepted the volume axis at two different volumes (Vo and Vu, respectively). The slopes of both ESPVR and EDPVR curves as well as Vo and Vu were variably influenced by positive and negative inotropic states, heart rate changes, arrhythmias, ischemia, and rigor. In control before any interventions, LV stroke and suction volume (delta V = Vu - Vo) at zero P was 7.5 +/- 2.5 (SD) ml/100 g left ventricle, which changed with the changes in Vo and Vu. delta V decreased with decreases in P from zero and virtually vanished at a pressure (Pn) of -9.5 +/- 2.0 mm Hg. Directly measured LV dead volume (Vd) at Pn was 4.1 +/- 1.3 ml/100 g. The results seem essential for evaluation of LV filling and suction during diastole.

Animals↗
PubMed1988

Crossbridge model compatible with the linear relation between left ventricular oxygen consumption and pressure-volume area.

Ventricular pressure-volume area (PVA) is a specific area in the pressure-volume diagram, which represents the total mechanical energy generated by each contraction, consisting of stroke work and mechanical potential energy at end-systole. Animal experiments have shown that PVA is correlated linearly with the ventricular oxygen consumption (Vo2) per beat under a variety of loading conditions in a stable contractile state. The slope of the Vo2-PVA line has been shown to remain constant in different contractile states, implying a constant stoichiometry between Vo2 and PVA. As a first step to understand the nature of this Vo2-PVA relation, we devised a new crossbridge (CB) model to theoretically relate PVA with the total enthalpy change associated with the ATP hydrolysis for all CB cycles. One of the most important assumptions on which this model analysis depended was that the time-varying elasticity model could simulate the instantaneous pressure-volume relation. The result of this analysis implied that the empirical linear Vo2-PVA relation could be attributed to the energy balance between energy input and output of the chemomechanical transduction associated with CB cycles during a ventricular contraction.

Cardiac Volume↗
PubMed1988

Incorporation of venous resistance in Togawa's four quadrant diagram for Guyton's circulatory equilibrium.

Guyton indicates that the contribution of venous resistance to venous return resistance is magnified by the compliance ratio (30) of the venous compartment to the arterial compartment. Therefore, even a slightly increased venous resistance sensitively decreases venous return and hence cardiac output in the circulatory equilibrium. However, Guyton's diagram does not allow an easy and explicit evaluation of the effect of venous resistance on cardiac output. The circulatory equilibrium can be visualized graphically by Togawa's four quadrant diagram. However, Togawa's diagram does not include venous resistance. Therefore, I modified Togawa's diagram to incorporate venous resistance in the first quadrant for the cardiac output curve. The new diagram shows easily and explicitly that venous resistance sensitively tilts down either the venous return curve or the cardiac output curve and markedly decreases venous return and cardiac output.

Cardiac Output↗