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PubMed2000

Postextrasystolic contractile decay always contains exponential and alternans components in canine heart.

In isolated, blood-perfused canine hearts, postextrasystolic potentiation (PESP) decays monotonically after a noncompensatory pause following a spontaneous extrasystole (ES). The monotonic PESP decay yields myocardial internal Ca(2+) recirculation fraction (RF). We have found that after a compensatory pause (CP), PESP decays in alternans, consisting of an exponential and a sinusoidal decay component. We have proposed that this exponential component also yields RF. In the present study, we examined the reliability of this alternative method by widely changing the ES coupling interval (ESI), CP, and heart rate in the canine excised, cross-circulated left ventricle. We found that all PESP decays consisted of the sum of an exponential and a sinusoidal decay component of variable magnitudes whether a CP existed or not. Their decay constants as well as the calculated RF were independent of the ESI and CP. This confirmed the utility of our alternative RF determination method regardless of the ESI, CP, and heart rate. Direct experimental evidence of Ca(2+) dynamics supportive of this alternative method, however, remains to be obtained.

Animals↗
PubMed2000

NO is involved in MCh-induced accentuated antagonism via type II PDE in the canine blood-perfused SA node.

The possible role of type II (cGMP-stimulated cAMP hydrolysis) phosphodiesterase (PDE) in the accentuated antagonism of muscarinic effects on heart rate during beta-stimulation via endogenous nitric oxide (NO) was evaluated. The canine isolated sinoatrial node preparation was cross circulated with arterial blood of a support dog. The sinoatrial rate of the preparation was 96 +/- 5 beats/min (n = 16) at control. Methacholine (MCh; 0.01-1 microg) injected into the right coronary artery in a bolus fashion caused dose-dependent decreases in sinoatrial rate. Under an intra-arterial infusion of isoproterenol (1 microM), resulting in approximately 50% increase in sinoatrial rate, MCh-induced decreases were markedly augmented from -18 +/- 3% to -44 +/- 4% at 0.3 mg of MCh. When N(G)-nitro-L-arginine methyl ester (100 microM) or N(G)-monomethyl-L-arginine (100 microM) were continuously infused, the augmented MCh-induced decreases in sinoatrial rate were significantly suppressed (-29 +/- 3% or -25 +/- 3%, respectively, P < 0.01). Pretreatment with either 3-isobutyl-1-methylxanthine (IBMX; 20 microM), a non-selective PDE inhibitor, or amrinone (20 microM), a selective type III (cGMP inhibited cAMP hydrolysis) PDE inhibitor, doubled the isoproterenol-induced increase in the sinoatrial rate. However, the augmented MCh-induced decreases in sinoatrial rate were significantly depressed by IBMX (from -23 +/- 5% to -14 +/- 1%, P < 0.01) but not by amrinone (to -20 +/- 3%). These results suggest that MCh-induced accentuated antagonism in the sinoatrial node pacemaker activity can be modulated by endogenous NO via an activation of the type II cyclic GMP-stimulated cAMP PDE.

Acetylcholine↗
PubMed2001

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of alpha-fodrin.

The aim of the present study was to examine the mechanisms of Ca2+ overload-induced contractile dysfunction in rat hearts independent of ischemia and acidosis. Experiments were performed on 30 excised cross-circulated rat heart preparations. After hearts were exposed to high Ca2+, there was a contractile failure associated with a parallel downward shift of the linear relation between myocardial O(2) consumption per beat and systolic pressure-volume area (index of a total mechanical energy per beat) in left ventricles from all seven hearts that underwent the protocol. This result suggested a decrease in O(2) consumption for total Ca2+ handling in excitation-contraction coupling. In the hearts that underwent the high Ca2+ protocol and had contractile failure, we found marked proteolysis of a cytoskeleton protein, alpha-fodrin, whereas other proteins were unaffected. A calpain inhibitor suppressed the contractile failure by high Ca2+, the decrease in O(2) consumption for total Ca2+ handling, and membrane alpha-fodrin degradation. We conclude that the exposure to high Ca2+ may induce contractile dysfunction possibly by suppressing total Ca2+ handling in excitation-contraction coupling and degradation of membrane alpha-fodrin via activation of calpain.

Animals↗
PubMed1977

Lost mass and excretion as stimuli to parabiotic compensatory renal hypertrophy.

To help determine the roles of lost renal mass and lost excretory ability in producing renoprival hypertrophy, observations were made in otherwise normal rats cross-circulated for 24 h with rats prepared in one of the following ways: bilateral nephrectomy, bilateral ureteral ligation, or bilateral nephrectomy with 24 h of uremia. Bilateral nephrectomy produced parabiotic increases in renal mass and in the average cellular concentration of RNA: bilateral ureteral ligation did not. Uremia did not potentiate the effects of bilateral nephrectomy. Lost mass is the determinant of compensatory renal hypertrophy.

Animals↗
PubMed2001

Impaired distensibility of the left ventricle after stiffening of the right ventricle.

Acute and chronic alterations of right ventricular (RV) wall properties can change left ventricular (LV) performance. We investigated whether and how stiffening of the RV free wall alters LV diastolic distensibility. We used cross-circulated isolated hearts, in which the LV and RV were independently controllable. Stiffness of the RV free wall was altered by intramuscular injections of glutaraldehyde into the RV free wall after right coronary artery ligation. We measured circumferential and longitudinal regional lengths in the septum and LV free wall. During data acquisition, RV volume was held constant. After the RV free wall was stiffened by glutaraldehyde, the LV diastolic pressure-volume relation shifted upward and became steeper. Importantly, stiffening of the RV free wall increased the diastolic regional area in the septum and LV free wall under constant LV volume. The augmented regional dimensions may result in enhanced regional tension under constant LV volume and may be related to the observed increase in LV diastolic intracavitary pressure. The impaired LV diastolic distensibility by stiffening of the RV free wall may be at least partly explained by myocardial stretch, probably due to LV deformation.

Animals↗
PubMed1975

Electrical and mechanical activity of the isolated canine stomach perfused with homologous, in vitro, oxygenated blood.

Electrical and mechanical activity was recorded from six totally isolated canine stomachs perfused with homologous blood oxygenated in vitro. Reactions to electrical vagal stimulation to cholinergic drugs and to pentagastrin were recorded. Electrical control activity, electrical response activity and mechanical response of isolated stomachs, observed in this in vitro system, were identical to those found in canine-isolated stomachs perfused with cross-circulated blood of living animals. It appears that when a living animal is included in the perfusion system of the isolated stomach, drugs used for gastric stimulation are rapidly metabolized and, due to this physiological clearance, repeated injections of stimulants can be given for several hours. Using the in vitro perfusion system, as in this experiment, injected drugs accumulate in the perfusion blood, as no clearance mechanism is available. Partial or total exchange of perfusion blood is therefore recommended. With these reservations, the in vitro system appears to be an easy method for the study of nonstimulated and stimulated electrical and mechanical activity of the totally isolated canine stomach.

Animals↗
PubMed2003

Mechanism of ST elevation and ventricular arrhythmias in an experimental Brugada syndrome model.

BACKGROUND: Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited. METHODS AND RESULTS: We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35x30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a KATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other. CONCLUSIONS: Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT.

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↗
PubMed1992

Mechanoenergetic effects of pimobendan in canine left ventricles. Comparison with dobutamine.

BACKGROUND: We hypothesized that the effect of pimobendan (UD-CG 115 BS) to increase calcium sensitivity of contractile protein might result in less myocardial oxygen consumption (VO2) in comparison with dobutamine when they enhance ventricular contractility to the same extent. To examine this hypothesis, we compared the effects of pimobendan and dobutamine on left ventricular contractility and energetics using the frameworks of Emax (contractility index) and the relation between VO2 and PVA (systolic pressure-volume area, a measure of left ventricular total mechanical energy). METHODS AND RESULTS: We measured VO2, Emax, PVA, and force-time integral (FTI) in excised, cross-circulated, nonfailing dog hearts. The slope of the VO2-PVA relation reciprocally indicates the efficiency from PVA-dependent VO2 to the total mechanical energy (contractile efficiency). The VO2 intercept of the VO2-PVA relation, i.e., PVA-independent VO2, reflects energy utilization for excitation-contraction coupling. The ratio of FTI to PVA-dependent VO2 can be called contractile economy. Both drugs comparably enhanced Emax. Although the contractile economy was greater by 14 +/- 19% (p less than 0.05) for pimobendan than for dobutamine, the contractile efficiency was similar between the two drugs. Oxygen cost of contractility, defined as the slope of the relation between the PVA-independent VO2 and Emax, was the same between the two drugs. Other mechanoenergetic effects of both drugs were similar except for a greater coronary vasodilating effect of pimobendan. CONCLUSIONS: Pimobendan has almost the same mechanoenergetic effects as dobutamine but slightly greater contractile economy and coronary vasodilation. The calcium-sensitizing effect of pimobendan did not save the oxygen cost of contractility.

Animals↗
PubMed1995

Logistic time constant of isovolumic relaxation pressure-time curve in the canine left ventricle. Better alternative to exponential time constant.

BACKGROUND: The time constant of left ventricular (LV) relaxation derived from a monoexponential model has been widely used as an index of LV relaxation rate or lusitropism, although this model has several well-recognized problems. In the present study, we proposed a logistic model and derived a "logistic" time constant (TL) as a better alternative to the conventional "exponential" time constant (TE). METHODS AND RESULTS: A total of 189 beats (147 isovolumic and 42 ejecting beats) were investigated in seven canine excised cross-circulated heart preparations. We found that the logistic model fitted much more precisely all the observed LV isovolumic relaxation pressure-time [P(t)] curves than the monoexponential model (P < .05). The logistic model also fitted well both the time curve of the first derivative of the observed P(t) (dP/dt) and the dP/dt-P(t) phase-plane curve. Like TE, TL indicated that volume loading depressed LV lusitropism and that increasing heart rate and ejection fraction augmented it. TL was independent of the choice of cutoff point defining the end of isovolumic relaxation; TE was dependent on that choice. CONCLUSIONS: We conclude that the logistic model better fits LV isovolumic relaxation P(t) than the monoexponential model in the present heart preparation. We therefore propose TL as a better alternative to TE for evaluating LV lusitropism.

Animals↗
PubMed1998

Relative efficacy of monophasic and biphasic waveforms for transthoracic defibrillation after short and long durations of ventricular fibrillation.

BACKGROUND: Recently, interest has arisen in using biphasic waveforms for external defibrillation. Little work has been done, however, in measuring transthoracic defibrillation efficacy after long periods of ventricular fibrillation. In protocol 1, we compared the efficacy of a quasi-sinusoidal biphasic waveform (QSBW), a truncated exponential biphasic waveform (TEBW), and a critically damped sinusoidal monophasic waveform (CDSMW) after 15 seconds of fibrillation. In protocol 2, we compared the efficacy of the more efficacious biphasic waveform from protocol 1, QSBW, with CDSMW after 15 seconds and 5 minutes of fibrillation. METHODS AND RESULTS: In protocol 1, 50% success levels, ED50, were measured after 15 seconds of fibrillation for the 3 waveforms in 6 dogs. In protocol 2, defibrillation thresholds were measured for QSBW and CDSMW after 15 seconds of fibrillation and after 3 minutes of unsupported fibrillation followed by 2 minutes of fibrillation with femoral-femoral cross-circulation. In protocol 1, QSBW had a lower ED50, 16.0+/-4.9 J, than TEBW, 20.3+/-4.4 J, or CDSMW, 27.4+/-6.0 J. In protocol 2, QSBW had a lower defibrillation threshold after 15 seconds, 38+/-10 J, and after 5 minutes, 41.5+/-5 J, than CDSMW after 15 seconds, 54+/-19 J, and 5 minutes, 80+/-30 J, of fibrillation. The defibrillation threshold remained statistically the same for QSBW for the 2 fibrillation durations but rose significantly for CDSMW. CONCLUSIONS: In this animal model of sudden death and resuscitation, these 2 biphasic waveforms are more efficacious than the CDSMW at short durations of fibrillation. Furthermore, the QSBW is even more efficacious than the CDSMW at longer durations of fibrillation.

Animals↗
PubMed1977

Effects of stroke volume and velocity of ejection on end-systolic pressure of canine left ventricle. End-systolic volume clamping.

To study the effects of contraction mode on ventricular end-systolic pressure-volume relationship, we compared the end-systolic pressure of isovolumic contraction with that of ejecting contraction at an identical end-systolic volume. The left ventricle of excised cross-circulated canine hearts was fitted with a water-filled balloon. The balloon was connected to a hydraulic pump that allowed the ventricle to contract to a preset constant end-systolic volume (19-37 ml) from a variable end-diastolic volume. At each of control, enhanced, and depressed levels of contractility, differences of end-systolic pressures of steady state isovolumic and ejecting contractions were evaluated while stroke volume and velocity of ejection were widely varied. The end-systolic pressure in the ejecting contraction tended to decrease by 5-15% from that of the isovolumic beat with increases in either stroke volume to 20-25 ml or peak velocity of ejection to about 800 ml/sec. There was no obvious difference in the results at different levels of contractility. The magnitude of the end-systolic pressure depression due to ejection was, however, relatively small as compared to 4-fold changes in end-systolic pressure due to the changes in contracility. We, therefore, conclude that the ventricular end-systolic pressure-volume relationship is affected slightly by ejection, and that this effect is much smaller than the maximal effect of changing contractility on the end-systolic pressure-volume relationship.

Animals↗
PubMed1981

The effect of right ventricular filling on the pressure-volume relationship of ejecting canine left ventricle.

Acute shifts in the pressure-volume relationship of the left ventricle occur under several conditions. One potential mechanism for this phenomenon is ventricular interdependence, that is, the influence of right ventricular filling on the left ventricle. This mechanism was studied in an isolated cross-circulated ejecting canine heart preparation with balloons sewn into both right and left ventricles and connected to volumetric chambers allowing continuous and accurate simultaneous measurement of right and left ventricular pressures and volume. Sets of left ventricular pressure-volume loops were obtained under a variety of right ventricular volumes. Experiments were repeated with and without the pericardium. Both diastole and systole were studied. We show that in the pericardium-free heart working over a normal range of volumes, the right ventricle exerts little influence on left ventricular pressure. With the pericardium present, there is a small but significant effect of right ventricular volume on left ventricular pressure during systole and diastole. Over a wider range of volumes imposed in the arrested heart, the right ventricle does influence left ventricular pressure even without the pericardium. Thus we have demonstrated that ventricular interdependence is not likely to lead to large acute pressure-volume shifts, either during diastole or systole, except in the presence of considerably above normal right ventricular volumes.

Animals↗
PubMed1982

Effects of coronary arterial pressure on left ventricular end-systolic pressure-volume relation of isolated canine heart.

In the excised canine left ventricle, the end-systolic pressure-volume relationship (ESPVR) has been shown to be approximately linear over the working range of loading conditions when coronary arterial pressure (CAP) is maintained constant, independent of loading conditions. To investigate the ESPVR under the more intact physiological condition in which the CAP varies with loading on the left ventricle, we studied the effect of changes in CAP on the ESPVR in 10 excised cross-circulated canine ventricles which were contracting isovolumically. The ESPVR, determined from isovolumic contractions at four different volumes, was reasonably independent of CAP as long as CAP remained above a critical pressure (67.0 +/- 22.1 mm Hg). Below this pressure, the slope of ESPVR decreased although the volume axis intercept (V0) remained unaltered. These findings indicate that under physiological conditions, where there is a close coupling of CAP to systolic left ventricular pressure, the ESPVR should become nonlinear in the low preload or afterload regions. When CAP was varied with the left ventricular pressure in five ventricles, the ESPVR indeed became nonlinear in the low-load region. We conclude that the ESPVR in intact conditions is reasonably linear in the physiological load range, but it can be nonlinear in the low-load range.

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↗
PubMed1987

Force-time integral decreases with ejection despite constant oxygen consumption and pressure-volume area in dog left ventricle.

We have shown that systolic pressure-volume area (PVA), which is equivalent to the total mechanical energy generated by ventricular contraction, correlates linearly with myocardial oxygen consumption, VO2, in canine left ventricle. Systolic force-time integral, FTI, also correlates with VO2. In this study, stroke volume was increased from 0 (isovolumic) in isolated cross-circulated canine left ventricle in a stable contractile state while keeping PVA constant with a servo pump. Ventricular total force was calculated from ventricular pressure and volume by the force-equilibrium equation and was integrated from the end of diastole to the end of systole as identified with the time of Emax to yield FTI. Under the conditions of constant PVA, FTI significantly (p less than 0.001) decreased by 10 +/- 7% and 25 +/- 8% with increases in stroke volume from 0 to 8 +/- 4 ml and 17 +/- 3 ml and in ejection fraction from 0 to 0.24 +/- 0.10 and 0.61 +/- 0.05, respectively, while VO2 and Emax remained constant. Therefore, we conclude that in a stable contractile state, it is possible to keep PVA constant even when stroke volume and ejection fraction are varied and that under such conditions, FTI no longer predicts VO2. PVA remains a reliable predictor of VO2 regardless of ventricular loading conditions.

Animals↗
PubMed1988

Dependence of instantaneous transfer function on regional ischemic myocardial volume.

To obtain the instantaneous left ventricular transfer function curve (instantaneous TFC) under conditions of regional ischemia, sinusoidal accelerations ranging from 30 to 150 Hz were applied to a small area of the epicardium of cross-circulated isovolumic canine left ventricle, and the contralateral acceleration was measured under control and during regional coronary occlusion (n = 11). The TFC is the ratio of the output to input acceleration amplitudes. The instantaneous TFC was characterized as a single-peaked configuration under control coronary perfusion. However, TFCs progressively changed from a single-peaked to a double-peaked configuration during regional ischemia. To quantify this change in instantaneous TFC, we defined an index D as the mean squared difference of TFC during ischemia from TFC during control. Index D was linearly related to the percent mass of the ischemic region at 40 minutes after onset of ischemia. We conclude that 1) transfer function curves are sensitive measures of myocardial heterogeneity and 2) the fractional ischemic weight of the ventricle is a major factor in determination of the deformation in instantaneous TFC at the later stages of regional ischemia.

Animals↗
PubMed1989

Time-invariant oxygen cost of mechanical energy in dog left ventricle: consistency and inconsistency of time-varying elastance model with myocardial energetics.

We studied whether the oxygen cost of mechanical energy is time-invariant in the excised, cross-circulated canine heart. The total mechanical energy generated by ventricular contraction can be quantified by the total pressure-volume area (PVA) according to the time-varying elastance model. In this model, mechanical energy generated until a specified time (t) during systole can be quantified by the partial pressure-volume area, PVA(t). PVA(t) was obtained by quickly releasing ventricular volume at a varied time during isovolumic contraction. The quick release aborted further development of mechanical energy. We found that PVA(t) at a constant end-diastolic volume linearly correlated with myocardial oxygen consumption (VO2). This indicates that the oxygen cost of mechanical energy is time-invariant. However, we also found that the slope of the VO2-PVA(t) relation decreased with increasing quick-release speed. This indicates a decrease in VO2 by the quick release despite the same PVA(t). The time-invariant oxygen cost of mechanical energy is consistent with the time-varying elastance model of the ventricle, but the decreased VO2 with increasing quick-release speed despite the same PVA(t) is not.

Animals↗