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Biomedical subjects

Y Ohgoshi

Publications and source records attributed to Y Ohgoshi.

29 records · Page 2Linked to original sources
PubMed1991

Denopamine (beta 1-selective adrenergic receptor agonist) and isoproterenol (non-selective beta-adrenergic receptor agonist) equally increase heart rate and myocardial oxygen consumption in dog heart.

The effects of denopamine (a beta 1-selective adrenergic receptor agonist) and isoproterenol (a non-selective beta-adrenergic receptor agonist) on heart rate, left ventricular contractility, and left ventricular oxygen consumption (VO2) at the same left ventricular volume were compared in excised cross-circulated dog hearts. Denopamine and isoproterenol increased heart rate and VO2 to a comparable extent at a comparably increased contractility. Moreover, the oxygen cost of contractility which quantifies VO2 for excitation-contraction coupling was the same between the two agents. These findings contradict the previously reported smaller increases in heart rate and VO2 by denopamine than by isoproterenol in open-chest dog hearts, which have been mainly attributed to the beta 1-selectivity of denopamine. Our results suggest that in isolated and denervated hearts, the degree of beta 1-selectivity of a beta-agonistic agent does not directly determine the relative potencies of its inotropic and chronotropic effects and the oxygen cost of contractility.

Adrenergic beta-Agonists↗
PubMed1991

Equivalent heart rate during ventricular fibrillation in the dog heart: mechanoenergetic analysis.

We propose equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual myocytes in a fibrillating ventricle by analyzing mechanics and energetics of the ventricle. Using the isolated, cross-circulated dog heart preparation, we determined eHR in two different ways. First, we obtained eHR (eHR1) from myocardial O2 consumption (Vo2)-equivalent pressure-volume area (ePVA) data points during ventricular fibrillation (VF) by utilizing the Vo2-pressure-volume area (PVA) relation in the beating state. PVA is the area surrounded by the end-systolic and end-diastolic pressure-volume relations and the systolic pressure-volume trajectory in the pressure-volume diagram. PVA has been shown to represent the total mechanical energy generated by each contraction. We have recently proposed ePVA as a measure of the total mechanical energy generated by single contractions of all individual asynchronously contracting myocytes in a fibrillating ventricle. ePVA is the area surrounded by the horizontal line at the VF pressure and the end-systolic and end-diastolic pressure-volume relations in the beating state. Second, we measured Vo2 in beating state at various heart rates and Vo2 during VF under a mechanically unloaded condition. By comparing these fibrillating and beating Vo2 values, we determined eHR (eHR2) for the fibrillating state. eHR1 was 216 +/- 27 beats/min and eHR2 was 223 +/- 26 beats/min. These two values were not significantly different. We conclude that the average frequency of contractions of individual myocytes in a fibrillating ventricle is equivalent approximately to 220 beats/min in terms of ventricular energetics.

Animals↗
PubMed1990

Force-time integral does not improve predictability of cardiac O2 consumption from pressure-volume area (PVA) in dog left ventricle.

We have proposed the systolic pressure-volume area (PVA) as a measure of the total mechanical energy generated by ventricular contraction, and we found a closely linear correlation between PVA and cardiac oxygen consumption (VO2). Although the force-time integral (FTI) has long been considered to be the most reliable correlate of cardiac oxygen consumption (VO2), we have already shown that VO2 remained constant although FTI was changed while PVA was kept constant in the excised, cross-circulated dog left ventricle. This means that PVA is superior to FTI as a predictor of VO2. In the present study, we studied whether a linear addition of FTI to PVA could improve the prediction of VO2 from PVA in isovolumic and ejecting contractions with different afterload pressures in the same type of dog left ventricle preparation. Although left ventricular VO2 was always closely correlated with either PVA (r = 0.967, mean after z-transformation) or FTI (mean r = 0.925), multiple regression analysis indicated that PVA alone accounted for as much as 94% (mean) of the variance of VO2 and that FTI linearly added to PVA accounted for an additional few percent of the variance (statistically significant in less than half the cases). We conclude that the addition of FTI to PVA does not improve the predictability of VO2 from PVA in ordinary contractions.

Animals↗
PubMed1990

Simulation of mechanoenergetics of asynchronously contracting ventricle.

We simulated mechanoenergetics of ventricular asynchronous contraction using a model comprising two compartmentalized asynchronous time-varying elastic elements, E1 and E2. Their elastances [e1(t) and e2(t)] waxed and waned cyclically with a variable time lag (tau). The pressure-volume area (PVA1 or PVA2) circumscribed by the maximum (emax) and minimum e1(t) or e2(t) lines and the contracting pressure-volume trajectory of E1 or E2 quantifies the mechanical energy generated by a contraction of E1 or E2. Similarly, the PVA circumscribed by the resultant Emax (ventricular contractility index) line, the end-diastolic pressure-volume (P-V) line, and the systolic P-V trajectory quantifies the mechanical energy of the entire ventricle. PVA of the ventricle is equal to the sum of PVA1 and PVA2. We found that Emax decreased with increases in tau despite constant emax, and hence ventricular PVA decreased with increases in tau. This simulation helps us to better understand the mechanism of decreased oxygen consumption with increasing ventricular asynchrony reported in the literature.

Animals↗
PubMed1990

New method to determine oxygen cost for contractility.

We developed a new method to determine the oxygen cost for myocardial contractility and applied it to epinephrine in the excised cross-circulated dog heart. We utilized the relation between myocardial oxygen consumption (VO2) and the systolic pressure-volume area (PVA) which represents the total mechanical energy generated by contraction. We first obtained a reference VO2-PVA relation in a baseline contractile state. Then, the end-diastolic and stroke volumes were fixed constant and a global index of ventricular contractility, Emax, was enhanced by infusing epinephrine. The VO2-PVA data point was shifted linearly right-upward with the increases in Emax. From the slopes of both the reference VO2-PVA relation line and the regression line of VO2 on PVA during the gradually increased Emax, we calculated the oxygen cost for contractility, i.e., the ratio of the elevation of the VO2-PVA relation to enhanced Emax in each heart. The ratio was 0.00095 +/- 0.00013 ml O2.ml.mmHg-1.beat-1.100 g LV-2. The result indicates that the oxygen cost for contractility can be reliably and efficiently determined by this new method.

Animals↗
PubMed1990

Comparison between Bretschneider's total myocardial energy demand (Et) and our total mechanical energy (PVA) as a predictor of cardiac oxygen consumption in dogs.

We compared the predictive capability of two indexes of ventricular oxygen consumption (VO2) in excised cross-circulated dog hearts. One of the indexes was Bretschneider's Et, formulated as the sum of energies for 5 different mechanical and nonmechanical activities of myocardium. The other one was the left ventricular systolic pressure-volume area (PVA), originally proposed by Suga. PVA is a measure of total mechanical energy and has been combined with Emax (ventricular contractility index) to predict VO2 in different inotropic states. When all data sampled from different hearts under various loading and inotropic conditions were pooled, both VO2 (Bret) predicted from Bretschneider's index and VO2 (Suga) predicted from Suga's index correlated well with the measured VO2 (VO2 (Measured)). However, VO2 (Bret) was more affected by the contraction mode as compared with VO2 (Suga), because the former includes ejection period as a parameter. Among the 5 terms of VO2 (Bret), the major correlate of VO2 (Measured) was found to be tension development energy term E3 which includes dP/dtmax as a parameter. VO2(Suga), as a predictive index of VO2 (Measured), was more reliable in each heart than in pooled data from all the hearts because of the interindividual variations of the coefficients. We conclude that both indexes have usefulness and limitations, and should be chosen depending on the application.

Animals↗
PubMed1990

Assessment of left ventricular regional work under ischemia.

The wall tension-regional area (T-A) loop method, a new approach assessing regional contractile function of the left ventricle, has been developed in experiments performed on the isolated dog heart. Regional work is quantitatively determined by the area within a T-A loop with physically correct dimensions of energy (Joule) and regional contractility can be reliably assessed by the end-systolic T-A relation (ESTAR). During global ischemia, both the T-A loop area and the slope of the linear ESTAR decreased in proportion to the decreases in left ventricular stroke work and contractility. During regional ischemia, the T-A loop area in an ischemic region decreased to near zero, and the ESTAR markedly shifted to the right with a decreased slope and an increased regional area intercept. In contrast, the T-A loop in a non-ischematic region showed an increase in systolic area shrinkage and a decrease in regional work, demonstrating hyperkinesis due to regional afterload reduction. In addition, the ESTAR in a non-ischemic region remained almost unchanged. Thus, using the T-A loop method we can reliably assess regional work and contractility of a left ventricular region under ischemia.

Animals↗
PubMed1989

Effect of ouabain on the relation between left ventricular oxygen consumption and systolic pressure-volume area (PVA) in dog heart.

We studied the effect of ouabain (digitalis) on the relation between left ventricular (LV) O2 consumption (VO2) and pressure-volume (P-V) area (PVA) in 7 excised cross-circulated canine heart preparations. PVA is a measure of the total mechanical energy generated by LV contraction and was obtained as the specific area in the P-V diagram circumscribed by the end-systolic P-V line, end-diastolic P-V curve, and the systolic P-V trajectory. Ouabain (0.11 mg, intracoronary-arterially) increased Emax (LV contractility index) by 58 +/- 44% (mean +/- SD) from 7.8 +/- 3.4 to 12.0 +/- 4.8 mmHg/(ml/100 g LV). PVA correlated linearly with LV VO2 per beat in either the control (r greater than 0.97) or the ouabain run (r greater than 0.96) in individual hearts. Ouabain increased the VO2-axis intercept of the regression line of VO2 on PVA from 0.029 +/- 0.004 in the control run to 0.036 +/- 0.009 ml O2/beat/100 g LV without significantly changing the slope [(1.53 +/- 0.24).10(-5) ml O2/(mmHg/ml)] of the regression line. This slope is equivalent to the contractile efficiency value of 44 +/- 6% from the excess VO2 above unloaded VO2 to PVA. The parallel elevation of the VO2-PVA relation with ouabain was similar to the results produced by epinephrine and Ca2+ in our previous studies. Ouabain, like epinephrine and Ca2+, did not change the contractile efficiency from the PVA-dependent fraction of VO2 to PVA.

Animals↗
PubMed1989

Arteriovenous oximeter for O2 content difference, O2 saturations, and hemoglobin content.

We combined two spectrophotometric oximeters to measure continuously and simultaneously arteriovenous O2 content difference (AVOD) as well as arterial and venous oxyhemoglobin saturations (SaO2, SvO2) and total hemoglobin concentration (Hb). AVOD of the flowing arterial and venous whole blood was determined by the method of Guyton et al. (J. Appl. Physiol. 10: 158-163, 1957) and Shepherd and Burgar [Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H437-H440, 1977]. The new arteriovenous oximeter was tested in dog experiments in which SaO2, SvO2, Hb, and AVOD were variously changed by temporary suffocation, electric muscle stimulation, hemorrhage and transfusion, and hemodilution with saline. AVOD, SaO2, SvO2, and Hb were compared with the data of the arterial and venous blood sampled near the oximeter cuvettes and measured with an IL282 CO oximeter. In one dog experiment and one in vitro blood experiment, AVOD data of the same arterial and venous blood were compared by connecting the present oximeter in series with an A-VOX Systems oximeter developed by Shepherd and Burgar. The results showed that the new arteriovenous oximeter can continuously measure AVOD, SaO2, SvO2, and Hb over wide ranges with reasonable accuracy.

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↗