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Biomedical subjects

O Yamada

Publications and source records attributed to O Yamada.

At least 217 records · Page 12Linked to original sources
PubMed1985

[A long-term prognosis of ventricular septal defect associated with aortic regurgitation].

Fifty-one cases of ventricular septal defect associated with aortic regurgitation (VSD and AR) were examined for past twenty-two years. Only VSD closure was performed for AR cases under Sellers II regurgitation. After the average of 11.6 years' follow-up, 14 cases retained over 60 mmHg of diastolic pressure and belonged to NYHA functional class 1. VSD closure and aortic cusp suspension were performed for AR cases over Sellers II regurgitation. Three cases operated before 1969 died of cardiac failure and one case recently died of infectious endocarditis (IE). Because of residual AR, one case was performed re-aortic cusp suspension one year after the operation and another case was scheduled for re-aortic cusp suspension after three years and eight months. Eighteen cases with malfunctioned valve caused by calcification, etc. underwent the aortic valve replacement. Early death was due to low cardiac output syndrome (LOS). Five cases were followed up for eleven years on the average. Two cases were found atrial fibrillation and myocardial infarction, respectively. Four cases were VSD + AR with the past history of IE and one died of LOS after surgery. Two cases were postoperative IE. One died three months after the operation and the other is doing well after the re-surgery by translocation. A long-term finding of SV1 + RV5 by electrocardiogram showed a significant decrease in left ventricular overload. Significant decrease of cardiothoracic ratio was observed in AR group under Sellers II regurgitation. Pulse pressure was significantly decreased as well.

Adolescent↗
PubMed1984

Oxygen consumption and pressure-volume area of abnormal contractions in canine heart.

Oxygen consumption rates (VO2) of isovolumic and normally ejecting contractions are closely correlated with their systolic pressure-volume areas (PVA) in a stable canine left ventricle. PVA is the area in the pressure-volume (PV) diagram that is circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop trajectory. We studied whether VO2s of abnormally loaded ejecting contractions were similarly correlated with their PVAs. Various abnormally ejecting contractions were produced in the left ventricle of the cross-circulated canine heart. VO2 and PVA data of the various abnormal contractions and the isovolumic and normally ejecting contractions were pooled together, to which the correlation and regression analyses were applied. They could be fitted by a linear regression analyses were applied. They could be fitted by a linear regression line with a high correlation coefficient and a slight scatter in each heart. We therefore conclude that PVA is the primary correlate of VO2, not only in the isovolumic and normally ejecting contractions but also in various abnormally loaded contractions in a given canine left ventricle with a stable contractile state.

Animals↗
PubMed1984

Independence of myocardial oxygen consumption from pressure-volume trajectory during diastole in canine left ventricle.

We have found that myocardial oxygen consumption is linearly correlated with the systolic pressure-volume area in the canine left ventricle. This pressure-volume area is a specific area in the pressure-volume diagram that is circumscribed by the end-systolic pressure-volume relation line, the end-diastolic pressure-volume relation curve, and the systolic segment of the pressure-volume trajectory. This area is equivalent to the total mechanical energy generated by ventricular contraction, consisting of the external mechanical work and the mechanical potential energy. In the present study, we specifically changed the course of the diastolic segment of the pressure-volume trajectory without changing the systolic segment of the pressure-volume trajectory and the systolic pressure-volume area. Although the fractions of external mechanical work and mechanical potential energy in the pressure-volume area were markedly changed, the simultaneously measured left ventricular oxygen consumption remained unchanged. This result indicates that the myocardial oxygen consumption is predominantly determined by the total mechanical energy generated during systole, or the systolic pressure-volume area, independent of how the total mechanical energy is converted effectively to external mechanical work during the cardiac cycle.

Animals↗
PubMed1984

Is regional ventricular wall work determined from regional force and shortening always consistent with the law of conservation of energy?

Contractile properties of a ventricular wall region have often been analyzed by regional force, shortening, and work. Regional force cannot be measured directly and is often indirectly determined from ventricular pressure and geometry, although regional shortening can be measured directly. Regional work can be calculated from these force and shortening values. We examined whether the calculated regional work, which may be mechanically reasonable, is also reasonable from an energetics viewpoint. We calculated regional contractile power (time rate of work) from the regional force and shortening velocity and integrated it globally over the entire ventricular wall, using some conventional geometric models of the ventricle and assumptions of ventricular wall mechanics. We then compared this globally integrated power with the stroke power of the entire ventricle determined directly from ventricular pressure and volume. Results show that the globally integrated regional power is not always identical with stroke power, depending on the model and assumptions used. Therefore, the regional ventricular wall work determined from the regional force and shortening is not always consistent with the law of conservation of energy.

Humans↗
PubMed1984

Normalization of end-systolic pressure-volume relation and Emax of different sized hearts.

A shift of the ventricular end-systolic pressure-volume (P-V) relation and a change in its slope Emax reasonably reflect a change in contractility in a given ventricle. However, comparison of Emax's of different sized hearts may be difficult without an appropriate normalization. We attempted to normalize Emax of different sized hearts to the force-length (F-L) relation of unit mass of myocardium in the ventricular wall. We formulated the end-systolic P-V relation as (end-systolic pressure) = Emax (end-systolic volume Vi - Vd), where Vd = volume axis intercept of the end-systolic P-V relation line. As a first step, both thick wall sphere and cylinder models of the ventricle with a wall volume of Vm were used. Circumferential F-L relation of unit myocardium in different ventricular wall layers were formulated as functions of Emax, Vd, and Vm. We found that as long as the product of Emax and Vd remains constant, the F-L relation in the midwall layer and the average F-L relation in the wall remain relatively unchanged regardless of wide changes in Vm and Vi. The elevation of the F-L relation curve, which represents myocardial contractility, was found to change in proportion to Emax Vd, largely independent of Vm and Vi, or the size of the ventricle.

Cardiac Volume↗
PubMed1984

Constant mechanical efficiency of contractile machinery of canine left ventricle under different loading and inotropic conditions.

We have recently proposed that the total mechanical energy generated in each cardiac contraction can be quantified by the systolic pressure-volume area (PVA). 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 trajectory. This area has dimensions of energy and comprises the external mechanical work and the elastic potential energy. In the left ventricle of cross-circulated canine hearts, we studied the relation between PVA and oxygen consumption per beat (VO2) above VO2 for mechanically unloaded contraction. We assumed that this excess VO2 is utilized for mechanical contraction by the contractile machinery. The percentage of PVA in the excess VO2, both in the same unit of energy, J, would then represent the efficiency of energy conversion from the excess VO2 to the total mechanical energy in the contractile machinery. We obtained this efficiency in variously loaded contractions in both control and enhanced contractile states with epinephrine and calcium. We found that the efficiency was constant at 30-50 (mean 40) % regardless of the changes in both loading conditions and contractile states. By this constant efficiency and a variable fraction of external work in PVA, we accounted for the load- and contractility-dependent variability of the conventional mechanical efficiency (0-30%) of the heart.

Animals↗
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

Frequency-selective auditory brain-stem response in newborns and infants.

The efficacy of the frequency-selective auditory brain-stem response (ABR) in new borns and infants was assessed using an auditory stimulus of a 1-kHz tone pip and compared with the results of click-evoked ABR. In subjects whose responses to conventional behavioral audiometry were obtained at intensities of 40 to 70 dB, the ABR thresholds evoked by 1-kHz tone pips and clicks lay between 5 and 20 dB hearing threshold level (HTL). In subjects who did not respond to conventional behavioral audiometry at the intensity of 70 dB, ABR thresholds in each auditory stimulus were elevated by 35 to 70 dB HTL, and no responses were noted at 80 to 90 dB HTL. These results indicate that frequency-selective ABR can be applied clinically as an objective method of audiometry for newborns and infants.

Acoustics↗
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↗