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Biomedical subjects

E L Yellin

Publications and source records attributed to E L Yellin.

At least 19 recordsLinked to original sources
PubMed1996

Time to dP/dtmax reflects both inotropic and chronotropic properties of cardiac contraction: a conscious dog study.

This study supports a mathematical model and previous findings indicating that td, the time from onset of contraction to dP/dtmax, reflects the time-dependent aspects of contraction and hence decreases with increasing contractility. Combined data from 20 conscious instrumented dogs create a highly significant inverse and linear td-HR (heart rate) relation. Both norepinephrine and isoproterenol decreased td values, but norepinephrine, in contrast to isoproterenol, decreased the heart rate by a reflex response. Despite the remarkable decline in heart rate (25.8%) td was decreased (16.5%). During wide spontaneous R-R variations longer preceding intervals gave shorter td values. The latter two facts indicate the dependence of td on the contractile state rather than it being merely interval dependent.

Adrenergic alpha-Agonists↗
PubMed1996

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

Animals↗
PubMed1996

Viscoelastic behavior of the isolated guinea pig left ventricle in diastole.

To determine left ventricular (LV) viscoelastic properties during acute volume changes, the relaxation of LV pressure (2-Fr, Millar) at steady LV volume after a known volume change was measured in 14 isolated guinea pig left ventricles arrested in diastole. The left ventricle was loaded and unloaded by manual injection and withdrawal of saline in 10 x 0.1-ml steps, controlling the steadiness of LV volume by measuring LV major and minor diameters (ultrasonic crystals). Cyclic stepwise volume loading and unloading resulted in a hysteresis loop, the complexity of which was caused by stress relaxation at each steady volume. With the use of linear regression analysis, the gross elastic effect of the pressure signal was separated from the viscoelastic part, decomposed into the fast and the slow component with time constants of relaxation equal to 1 and 20 s, respectively. The amplitudes of the fast and the slow component showed that 1) stress relaxation is more expressed at higher LV volume and 2) it is asymmetric, i.e., it is well expressed during volume loading and almost absent during volume unloading. Both suggest that viscoelasticity of passive myocardium is not quasilinear, when the left ventricle is subjected to aperiodic volume loading to a high LV volume. The asymmetric viscoelastic behavior is consistent with the hypothesis of extracellular fluid filtration.

Animals↗
PubMed1995

Origin of regional pressure gradients in the left ventricle during early diastole.

Left ventricular (LV) pressure (P)-diameter, LVP-area, or LVP-volume relationships used to evaluate LV diastolic function assume uniform LV wall motion and constant LVP. Contrary to these assumptions, there are significant differences in ventricular dynamic geometry and in LV pressures measured simultaneously in different parts of the LV, particularly during early diastole. We instrumented six anesthetized open-chest dogs with three pairs of orthogonal ultrasonic crystals (anterior-posterior and septal-free wall minor axes, and base-apex major axis) and two micromanometers (in the apex and in the LV base). The mitral valve occluder was implanted during standard cardiopulmonary bypass in the mitral annulus. Data were recorded during 11 transient vena caval occlusions. The mitral valve was occluded for 1 beat every 6-8 beats during each vena caval occlusion to produce nonfilling diastole. With the decrease of the LV end-systolic volume (Ves) below the equilibrium volume Veq (volume of the completely relaxed LV at LVP = 0); the minimum negative LVP in nonfilling beats increases, the shape of the ventricle is more ellipsoidal in both filling and nonfilling beats, and the base-to-apex pressure gradient at the time of LVP minimum increases regardless of the presence or absence of filling. Thus heterogeneous myocardial stresses during isovolumic relaxation and early diastole result in ventricular shape changes, intraventricular redistribution of chamber volume, local accelerations of blood, and associated intraventricular LVP gradients. The role of elastic recoil assumes greater importance at Ves smaller than Veq, when the left ventricle becomes more ellipsoidal in shape during isovolumic relaxation, leading, in turn, to greater shape changes and greater LVP gradient.

Animals↗
PubMed1995

Determination of vascular impedance in the peripheral circulation by transcutaneous pulsed Doppler ultrasound.

Instantaneous blood flow velocity characteristics and vascular impedance spectra derived noninvasively by pulsed Doppler ultrasound and invasively by electromagnetic flow probe were compared in the canine common femoral artery to validate the pulsed Doppler technique for determination of vascular impedance in the peripheral circulation. Although Doppler ultrasonography is routinely performed to evaluate blood flow velocity patterns in the human peripheral circulation; the validity of this technique to derive peripheral vascular impedance has yet to be investigated. Simultaneous measurements of blood flow velocity were determined by both noninvasive pulsed Doppler ultrasound and surgically implanted electromagnetic flow probe in the common femoral artery of eight dogs and compared in both time and frequency domains. Vascular impedance spectra derived from measurements of blood flow velocity determined by Doppler ultrasound and electromagnetic flow probe and simultaneous measurement of arterial pressure by a micromanometer-tipped catheter were obtained at baseline and after intra-arterial injection of acetylcholine in five additional dogs. During the first 10 to 20% of the cardiac cycle, Doppler ultrasound blood flow velocity was transiently greater than the simultaneously recorded electromagnetic blood flow velocity. During the remainder of the cardiac cycle, the two blood flow velocity waveforms were nearly superimposable. The frequency spectra of the blood flow velocity waveforms derived from Doppler ultrasound and electromagnetic flow probes were similar for harmonies less than 10 Hz. Vascular impedance spectra derived from measurements of blood flow velocity determined by Doppler ultrasound and electromagnetic flow probe with simultaneous measurement of arterial pressure by a micromanometer-tipped catheter were similar at baseline and after regional administration of acetylcholine. Mean vascular resistance (impedance at 0 Hz), characteristic impedance, and the first minima of the impedance modulus derived from Doppler ultrasound and electromagnetic flow probe blood flow velocity measurements were closely correlated at baseline and after dilation with acetylcholine (r > or = 0.89, p < 0.05 for all correlations). Doppler ultrasonography is a convenient and accurate technique for determination of vascular impedance in the peripheral circulation.

Animals↗
PubMed1994

Modeling the transient response to volume perturbations in the beating heart by the difference equation method.

Discrete theoretical methods, compatible with the discrete features of the beating heart, are used together with experimental study to attain a quantitative understanding of the transient response to a volume perturbation and of sustained mechanical alternans (SMA) in the beating heart. This is done in three stages. In stage A, a first-order difference equation describes the stroke volume (SV) response due to the Frank-Starling mechanism. It is shown that the value of gamma, the slope of the SV-end-diastolic volume curve, determines the type of response obtained because of a perturbation: 1) nonoscillatory decay for gamma < 1,2) oscillatory decay for 1 < gamma < 2, 3) SMA for gamma = 2, and 4) chaotic response for gamma > 2. In stage B, when the effect of each SV change on the successive end-diastolic aortic pressure (P) is considered, SV response to a perturbation is determined by a second-order difference equation. The solution of this equation shows that the response is determined by gamma and by the afterload factor lambda 1 = alpha 1.delta, where alpha 1 = delta Pj + 1/delta SVj and delta = delta SVj + 1/delta Pj + 1. The responses are a nonoscillatory decay for lambda 1 < 1 - gamma (type 1), oscillatory decay for 1 - (gamma/2) > lambda 1 > 1 - gamma (type 2), SMA for lambda 1 = 1 - gamma/2 (type 3), and 2:1 electrical-mechanical response for lambda 1 > 1 - gamma/2 (type 4). In stage C, a single volume perturbation, delta SVj, will directly affect not only Pj + 1 but also the subsequent values of P. Filling volume perturbations performed with a mitral valve occluder in eight anesthetized dogs led only to type 1 and 2 responses. The responses predicted by the model (using the experimental values of gamma and lambda 1) in each of the eight open-chest dogs are compatible with the experimental responses, suggesting that it is unlikely that SMA is initiated and maintained by variations in preload and afterload.

Animals↗
PubMed1994

Left atrial pressure-clamp servomechanism demonstrates LV suction in canine hearts with normal mitral valves.

A novel technique is presented to study suction of the in situ left ventricle in open-chest experimental animals without requiring cardiopulmonary bypass or disturbing the native mitral valvular apparatus. In 17 dogs, left ventricular pressure (LVP) and left atrial pressure (LAP) were measured, the left atrium was cannulated and connected to a servo pump, and LAP was controlled to a setpoint near 0 mmHg by withdrawing blood from the left atrium. Heart rate [103 +/- 17 (SD) min-1], peak pressure (100 +/- 13 mmHg), minimum pressure (1.4 +/- 0.8 mmHg), and maximum rate of change of pressure with respect to time during isovolumic contraction and relaxation (2,506 +/- 775 and -1,761 +/- 855 mmHg/s, respectively) were normal. Servo control of LAP was possible to +/- 1 mmHg. LV suction was demonstrated in each heart (mean negative LVP -2.3 +/- 1.1 mmHg; P < 0.0001). This new technique demonstrates that the left ventricle can generate negative diastolic suction pressures when examined in vivo and in situ with an undisturbed mitral valve and physiologically normal preload and afterload. This adds to a growing body of evidence that, under appropriate circumstances, the heart can suck blood into itself and thereby aid in its own filling.

Animals↗
PubMed1993

Studies on the safety of intrasplenic hepatocyte transplantation: relevance to ex vivo gene therapy and liver repopulation in acute hepatic failure.

Hepatocytes transplanted into the host liver engraft promptly, retain normal function, and survive indefinitely. Although intrasplenic transplantation is effective in delivering hepatocytes to the liver, to define potentially limiting complications, we studied its safety in normal, cirrhotic, and partial portal vein-ligated rats. In normal rats, portal pressures increased severalfold after hepatocyte transplantation but returned to normal within 3 weeks. In contrast, in portal hypertensive rats with partial portal vein ligation or cirrhosis, portal pressures were either unchanged or increased less after hepatocyte transplantation. However, more transplanted cells migrated to the lungs along with a rise in right atrial pressures in portal hypertensive rats. Further quantitative studies using 111Indium-labeled hepatocytes showed that intrasplenic retention of transplanted hepatocytes was similar in all animal groups. Intrahepatic cell translocation was comparable in normal and cirrhotic rats, whereas fewer cells migrated to the liver in partial portal vein-ligated rats. The most remarkable difference, however, was significantly greater intrapulmonary translocation of hepatocytes in portal hypertensive rats, which was presumably related to portosystemic shunting. These results indicate that because intrasplenic hepatocyte transplantation induces only temporary portal hypertension in normal subjects, potential strategies to augment liver repopulation could include repeated cell transplantation. This should be useful for optimizing the results of ex vivo gene therapy, or other hepatocyte-based therapies. However, the hepatic and portal hemodynamic status requires careful evaluation in portal hypertensive or cirrhotic subjects if serious complications are to be avoided.

Animals↗
PubMed1992

Diphenylhydantoin inhibits calcification of bovine pericardial implants and myocardium: a preliminary study.

Calcification is a major cause of glutaraldehyde-fixed bioprosthetic valve failure. Recent studies have shown that dystrophic calcification shares basic features with normal bone mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. In this study, we observed that calcification of the myocardium of DBA/2J mice was inhibited or reversed by diets supplemented with 100 mg/kg diet diphenylhydantoin (dilantin) for 70 days, with a calcification incidence of 25% in the dilantin group versus 58% in control. We further studied the effects of dilantin on bioprosthetic valve calcification. Three groups of young male Sprague-Dawley rats (100 g, 9/group) were implanted subcutaneously with 1-cm2 pieces of glutaraldehyde-fixed bovine pericardium. Controls were fed a ground chow for 45 or 90 days postimplantation; experimentals received the same chow for the first 45 days postimplantation and then were fed the same diet supplemented with 1000 mg dilantin/kg for the succeeding 45 days. Calcium content (microgram/mg dry weight) of the implants in the dilantin group was 137 +/- 18.6 versus 214 +/- 34.3 in 90 days control and 79.9 +/- 41.5 in 45 days control (mean +/- SD, P < 0.01 and P < 0.05 respectively, t test). The tibia calcium content of the dilantin group was not significantly different from 90 days control. We conclude that orally administered dilantin inhibits calcification of glutaraldehyde-fixed bovine pericardial implants preferentially. It does not cause decalcification either of implants that have already calcified or of the bones. The anti-calcification effect of dilantin may be associated with its anti-vitamin D effect.

Animals↗
PubMed1991

Atrial contribution to ventricular filling in mitral stenosis.

BACKGROUND: The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both. METHODS AND RESULTS: We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase. CONCLUSIONS: The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.

Adult↗
PubMed1991

Mechanism of sustained mechanical alternans. Effect of variations in ventricular billing volume.

This study investigations the phenomenon of sustained mechanical alternans (SMA) through the use of quantitative criteria. Discrete analysis is used to demonstrate that the hemodynamic variables during SMA are governed by a simple mathematical relation. The analysis shows that the value of the slope created by the two alternating beats on the stroke volume (SV)-end-diastolic volume (EDV) plane is gamma = (mu - 1) (1 + beta)/(mu - beta), where mu = SVs/SVw, and SVs and SVw denote the strong and weak beats, respectively, in the presence of one contractile state, and the beats associated with the higher and lower contractile states, respectively, in the presence of two alternating contractile states; beta = FVs/FVw, where FVs and FVw are the filling volumes after SVs and SVw, respectively. This equation is valid, whether SMA is exhibited in the presence of one or two contractile states and irrespective of the SV-EDV functional relation. Assuming constant afterload, a criterion based on this slope (gamma) is described to determine if SMA is caused by variations in EDV and FV. The slope of the SV-EDV curve in the presence of one contractile state (denoted as gamma) was determined directly (34 runs in eight dogs) by preventing FV in a beat, after a steady state, using a remote-controlled mitral valve. The slope gamma = 0.892 +/- 0.078 was found to agree with data in the literature. In 10 other dogs, mitral flow and aortic flow were measured in 55 series of SMA. In 51 series, gamma was greater than 1. Because the experimental slope in the presence of one contractile state, gamma, is smaller than or equal to 1, the possibility that one contractile state is involved in this series is rejected. On the other hand, when two contractile states are involved, the slope that the two successive beats create on the SV-EDV plane, gamma, is determined by connecting the two SV-EDV relations. This slope tends to be greater than 1. Thus, in these 51 series, SMA cannot be explained as a result of the Frank-Starling mechanism and variations in FV but as a result of two alternating contractile states. In the other four series, the value of gamma can be compatible either with the presence of one contractile state or with two alternating contractile states. This quantitative analysis enables the classification of the various types of SMA into subcategories with well-defined features. The quantitative analysis presented here shows that the common genesis of SMA is an alternating contractile state.

Animals↗
PubMed1990

Relationship between diastolic shape (eccentricity) and passive elastic properties in canine left ventricle.

This study was designed to investigate the relationship between left ventricular (LV) eccentricity, volume, and passive elastic properties. Eight open-chest fentanyl-anesthetized dogs were instrumented with an LV micromanometer, a remote-controlled mitral valve occluder, and two pairs of ultrasonic crystals to measure anterior-posterior and base-apex dimensions. We identified the presence of elastic recoil forces with negative LV diastolic pressure in nonfilling diastoles (end-systolic volume clamp). Using linear regression analysis we related midwall eccentricity to volume in nonfilling diastoles at the time of LVPmin and at end diastole, and in normal beats at end systole at LVPmin and at end-diastole. Intersection of the end-systolic and end-diastolic lines (transitional volume, Vt = 38.0 + 6.4 ml) divides cycles with and without the presence of elastic recoil forces. Vt is analogous to the equilibrium volume (V0), determined as the volume intercept of the logarithmic passive pressure-volume (P-V) relationship using LV volume estimated from LV weights (V0 nl = 37.6 + 4.4 ml), or the volume intercept of the linearized P-V relationship calculated from a prolate spheroidal model using measured minor and major diameters (V0 l = 44.5 + 3.5 ml). Linear regression analysis was also used to relate the square of peak mitral flow (MF2) with the corresponding atrioventricular pressure gradient (delta P); the slope represents a dissipative constant for the cycles without, P = 0.00058(MF)2 + 0.35 (n = 48, r = 0.73), and with elastic recoil P = 0.00035(MF)2 + 0.21 (n = 24, r = 0.81).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effect of early diastolic loading on myocardial relaxation in the intact canine left ventricle.

Early transmitral flow (MiF) patterns depend strongly on the rate of fall of measured left ventricular pressure (Pm) determined by both the active decay of pressure (Pa) due to myocardial relaxation and the increase in pressure due to stretch of passive elements during filling (Pp). This study was designed to uncouple passive forces from deactivation in order to reveal the instantaneous rate and duration of myocardial relaxation. We assumed a parallel combination of passive and active elements: Pm(t,V) = Pa(t) + Pp(V), with no constraints on the form of Pa(t), where t is time and V is ventricular volume. Pp(V) was determined by a retrospective analysis of data obtained in 11 anesthetized dogs instrumented for volume clamping with a remote-controlled mitral valve, with left atrial and left ventricular micromanometers, and with an electromagnetic probe to measure MiF. The passive pressure-volume relation (both positive and negative portions) was determined by clamping at end-systolic volume or after various filling volumes, and fit to logarithmic functions. Pp(t) was then calculated from Pp(V) and V(t) (integral of MiF). Time to end relaxation (Ter) was defined as time when Pa = 0. During isovolumic relaxation, when dPp/dt = 0, dPm/dt is equal to the relaxation rate, dPa/dt. In completely isovolumic relaxations, asymptote P infinity = -7 +/- 6 mm Hg (thus, Pa is 7 mm Hg greater than Pm) and Ter = 40 +/- 15 msec, compared with 175 +/- 53 msec during normal filling. In high versus low inotropic state, Pa at the beginning of filling was greater (18.1 +/- 6.1 vs. 12.2 +/- 3.9 mm Hg), and Ter was shorter (170 +/- 42 vs. 228 +/- 43 msec). Active pressure Pa(t) during filling is not an exponential function, and at any time, it was always greater after filling than in nonfilling beats, which indicates an increase in the relaxation duration. We conclude that myocardial relaxation is modulated by filling, which slows its rate and increases its duration, and is therefore a function of both ventricular volume and time. Such a mechanism may have an important role in regulating the diastolic pressure-volume relation.

Animals↗
PubMed1990

Diastolic viscous properties of the intact canine left ventricle.

The viscoelastic model of the ventricle predicts that the rate of change of volume (strain rate) is a determinant of the instantaneous pressure in the ventricle during diastole. Because relaxation is not complete before the onset of filling, one cannot distinguish the individual effects of relaxation and viscosity unless the passive and active components that determine the ventricular pressure are separated. To overcome this problem, we used the method of ventricular volume clamping to compare the pressures in the fully relaxed ventricle at a given volume at zero strain rate (static pressure) and high strain rate (dynamic pressure). Six open-chest, fentanyl-anesthetized dogs were instrumented with micromanometers and an electronically controlled mitral valve occluder in series with the electromagnetic flow probe. We reasoned as follows: If there were significant viscosity, then the dynamic pressure would be higher than the static pressure. The static pressure was measured when the ventricle was completely relaxed following a mitral valve occlusion after an arbitrary filling volume had been achieved. The dynamic pressure was determined by delaying the onset of filling until relaxation was complete and then measuring the pressure at the same volume that was achieved when the static pressure was measured. In 19 different hemodynamic situations, the dynamic and static pressures were identical (mean difference, 0.1 +/- 0.8 mm Hg), indicating that in the passive ventricle viscoelastic effects are insignificant and do not contribute to the left ventricular diastolic pressure under normal filling rates.

Animals↗
PubMed1989

Hemodynamic effects of high-frequency jet ventilation in dogs with a chronically banded pulmonary artery.

Two to seven weeks after banding the main pulmonary artery, the hemodynamic effects of high-frequency jet ventilation (HFJV) and conventional mechanical ventilation (CMV) were studied in dogs with and without PEEP. In comparison with CMV, HFJV significantly increased cardiac index, stroke index (SI), left ventricular stroke work index, and oxygen delivery index, and decreased pulmonary vascular resistance index both with and without PEEP; however, there were significant decreases in PaO2 and increases in intrapulmonary physiologic shunt ratio in HFJV without PEEP. SI without PEEP was significantly greater with HFJV when the peak airway pressure was synchronized with the diastole in pulmonary arterial pressure (PAP) than with CMV and with HFJV synchronized with the systole in PAP. These findings suggest that HFJV has hemodynamic advantages over CMV in dogs with chronically banded pulmonary artery and dilated right ventricle.

Airway Resistance↗