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H Suga

Publications and source records attributed to H Suga.

At least 163 records · Page 9Linked to original sources
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

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

Constant efficiency versus variable economy of cardiac contraction.

An intriguing aspect of cardiac mechanoenergetics is the smaller variability of the contractile efficiency than the energy economy of force. We theoretically speculated about this dissociation by relating the mechanical efficiency with Po/a (the curvature of the force-velocity curve) in Hill's characteristic equation of muscle; Po/a is known to change with the energy economy and inversely with Vmax and myosin ATPase activity. The analysis showed that the variability is smaller for the mechanical efficiency than for Po/a and that the energy economy changes approximately with (Po/a)3. These theoretical relations may partly explain the small variability of the empirically observed contractile efficiency under various experimental conditions which are known to widely change the energy economy.

Animals↗
PubMed1992

Modified hemoglobin solution as possible perfusate relevant to organ transplantation.

A modified hemoglobin solution ( - conjugate solution, PHP solution) has very interesting characteristics such as oxygen-carrying property without corpuscular components. Experimental use of the PHP solution has shown promising possibilities as a perfusate relevant to organ transplantations. 1) Elongation of warm ischemic time in canine kidneys: Dogs survived even with the unilateral kidneys which had been exposed up to 4.5 hour warm ischemia and, thereafter, perfused with the PHP solution. 2) Elongation of perfusion preservation period of canine livers: Dogs survived with the transplanted livers which had been perfused for 48 hours with the PHP solution. 3) Successful perfusion of rat small intestine: Lewis rat intestines perfused and preserved for 12 hours with the PHP solution showed a higher survival rate compared with those with Collins or UW solution. 4) Removal of antibodies: By exchange transfusion with a total of 30-60 ml of the PHP solution, a Lewis rat hematocrit lowered to 5% while IgG went down to nil from 8970 mg/dl, IgA to 28 mg/dl from 118 mg/dl and IgM to 190 mg/dl from 897 mg/dl. This technique is expected to be applicable for removal of the naturally existing antibodies in xenotransplantation.

Animals↗
PubMed1992

[Complications of emergency coronary angioplasty for acute myocardial infarction].

To assess the incidence and consequences of complications occurring during emergency percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI), we studied 347 patients who underwent PTCA within 24 hours after the onset of AMI. Acute occlusion occurred in 29 patients (8.4%), of whom 16 patients underwent successful repeat PTCA. All of them survived until hospital discharge. The in-hospital reocclusion rates of these 16 patients were comparable to those of patients who had not experienced acute occlusion (18.8 vs 12.8%, ns). In the remaining 13 patients, reperfusion were not successful after acute occlusion, and 6 died. Side branch occlusion occurred in 21 patients (6.1%). Left circumflex artery occlusion occurring during PTCA for the proximal left anterior descending artery was fatal in 3 patients. Right ventricular branch occlusion during PTCA for the middle of the right coronary artery resulted in intractable right ventricular infarction in one patient, and he died. Among 14 patients who underwent repeat angiography, 13 had a patent side branch which had been occluded during PTCA. One patient had coronary rupture and died. During PTCA of the proximal left anterior descending artery, acute occlusion of the artery without reperfusion or occlusion of the left circumflex artery was often fatal. However, the prognosis of acute occlusion was relatively good, if repeat PTCA was successful and most of the occluded side branches remained patent in the chronic state.

Aged↗
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

Group II phospholipase A2 inhibitors suppressed lysophosphatidylserine-dependent degranulation of rat peritoneal mast cells.

Rat peritoneal mast cells were sensitized with IgE and challenged with the specific antigen in the presence of lysophosphatidylserine (lysoPS), an essential co-factor for rodent connective tissue mast cell degranulation, and the effects of phospholipase A2 inhibitors were examined. Mepacrine, a known inhibitor of phospholipase A2, at concentrations below 10(-5) M and anti-rat 14-kDa group II phospholipase A2 antibody inhibited histamine release, while they did not affect the prostaglandin generation. Like histamine release, prostaglandin generation in IgE- and antigen- challenged rat peritoneal mast cells was dependent on the presence of lysoPS. These results indicate that 14-kDa group II phospholipase A2 may play an essential role in IgE-, antigen-, and lysoPS-dependent degranulation process of rat peritoneal mast cells and that the mechanism whereby it participates may not be due to the production of lysoPS from PS in mast cell membranes.

Animals↗
PubMed1991

Structural analyses of a channel-forming fragment of colicin E1 incorporated into lipid vesicles. Fourier-transform infrared and tryptophan fluorescence studies.

Structural changes upon binding to the membrane of a COOH-terminal channel-forming thermolytic fragment of colicin E1 have been studied by means of a variety of spectroscopic techniques. Circular dichroism measurements show that the thermolytic fragment predominantly takes a helical structure in aqueous and detergent solutions. Fourier transform infrared spectroscopic measurements indicate that the content of the beta-structure is significantly increased when the thermolytic fragment is bound to vesicles. On the basis of the result of tryptophan fluorescence measurements, we have concluded that each of the three tryptophan residues of the thermolytic fragment exists in different environments, i.e. one is buried in the lipid bilayer, one exists on the cis side of the vesicles, and one exists near the surface of the lipid bilayer. The Fourier transform infrared and fluorescence data have been used along with the crystal structure of colicin A, which is highly homologous to colicin E1 in structure and function, to propose a model of the thermolytic fragment bound to the lipid vesicles.

Amino Acid Sequence↗
PubMed1991

19F and 31P NMR spectroscopy of G protein alpha subunits. Mechanism of activation by Al3+ and F-.

19F and 31P NMR spectroscopy was used to study the mechanism of activation of the alpha subunits of guanine nucleotide-binding regulatory proteins (G proteins) by Al3+, Mg2+, and F-. 19F NMR spectra of solutions containing Al3+, Mg2+, and F- showed a characteristic F- peak at -10 ppm. Addition of the GDP-bound form of either of two G protein alpha subunits (G alpha) resulted in the appearance of an additional peak at -29 or -30 ppm. This peak was not observed with guanosine 5'-3-O-(thio)triphosphate-G alpha or with GDP alone. Titration of Al3+, Mg2+, and F- indicated that each molecule of G alpha binds 3-5 molecules of F- (Kd = 0.47 mM), a single molecule of Al3+ (Kd much less than 0.1 mM), and a single Mg2+ ion (Kd about 0.1 mM). Replacement of Mg2+ with Mn2+ caused a dramatic broadening of the NMR signal, indicating that the metal ion binds in proximity to the protein-bound F- (less than 1 nm). 31P NMR of GDP-G alpha showed peaks at -2 and -8.6 ppm, corresponding to the beta- and alpha-phosphoryl groups of GDP, respectively. Binding of Al3+, Mg2+, and F- caused an upfield shift of 6 ppm for the beta-phosphoryl signal with no change in the alpha-phosphoryl signal. These observations indicate that Mg2+.GDP.AlF3-5 mimics Mg2+.GTP in its capacity to activate G protein alpha subunits.

Aluminum↗
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

Hyperthyroid dog left ventricle has the same oxygen consumption versus pressure-volume area (PVA) relation as euthyroid dog.

We studied the effects of hyperthyroidism on the relation between O2 consumption (Vo2) and the pressure-volume area (PVA) of the left ventricle (LV) in dogs. PVA is a measure of the total mechanical energy generated per beat of LV. Dogs were treated by daily intramuscular injection of 0.3 or 1.0 mg/kg L-thyroxine over 2-5 weeks. Hyperthyroid dogs had a 40 times higher serum T4, a 40% higher sinus heart rate, and a 35% higher LV Emax (an index of ventricular contractility) than euthyroid dogs. Hyperthyroid dog hearts had linear Vo2-PVA relations like euthyroid dog hearts. The regression line was Vo2 = A x PVA + B, where A was 2.30 (dimensionless) and B was 0.53 J/beat per 100 g LV. B was significantly increased with dobutamine and decreased with propranolol, whereas A was not significantly changed by them. These A and B values were comparable to euthyroid data. Hyperthyroidism did not significantly affect myosin Ca-ATPase activity and V3-type myosin predominance, but increased the speed of the force transient response to length perturbation by 20%-70%, suggesting similar increases in crossbridge cycling rate. We conclude that in spite of accelerated crossbridge cycling rate the Vo2-PVA relation was not altered by hyperthyroidism in dogs.

Animals↗