Biomedical subjects

R E Mates

Publications and source records attributed to R E Mates.

14 recordsLinked to original sources

PubMed1991

Diastolic coronary resistance and capacitance are independent of the duration of diastole.

Systolic myocardial contraction may produce changes in coronary resistance and capacitance that persist throughout a normal diastole. In addition, coronary resistance and capacitance as determined in the arrested heart may not accurately describe normal diastolic behavior. To evaluate these possibilities, an identification method capable of characterizing the input impedance of the coronary circulation in as little as 150 ms was developed. Using this method, coronary dynamics were measured during early and late diastoles in the beating heart with tone intact as well as during adenosine-induced maximal vasodilation. Coronary dynamics were also measured in the arrested heart during maximal vasodilation. With vasomotor tone intact, the parameters of a lumped model of the coronary circulation showed no variation from early to late diastole. During maximal vasodilation, model parameters also showed no variation from early to late diastole. Parameters in the arrested heart were not statistically different from those of the beating heart during maximal vasodilation. However, model parameters determined during maximal vasodilation were significantly different from those determined with tone intact. These results suggest that although coronary resistance and capacitance are dependent on vasomotor tone, they remain constant throughout diastole and remain similar in the arrested heart.

Animals↗

PubMed1991

Coronary input impedance is constant during systole and diastole.

Although it is well known that coronary inflow decreases substantially during systole, the mechanism responsible for this decrease remains controversial. Knowledge of how coronary input impedance is affected by contraction can differentiate between some of the proposed mechanisms. In open-chest dogs, we have measured coronary inflow in the beating heart both during constant-pressure perfusion and during 10-Hz sinusoidal pressure oscillations around the same constant pressure. By exploiting the principle of superposition, we have shown that coronary input impedance remains unchanged between systole and diastole. Using this result, we have shown that a simple lumped-parameter model with constant resistance and compliance can describe coronary inflow at heart rates of 60, 90, 120, and 150 beats/min both with vasomotor tone intact and during maximal coronary vasodilation. Coronary resistance and compliance determined using the model are comparable to those obtained in our laboratory and by others during normal diastoles and in the arrested heart. The results suggest that, despite large increases in myocardial tissue stresses during systole, coronary resistance and compliance as determined using inflow measurements are constant during systole and diastole.

Animals↗

PubMed1991

Tone-dependent waterfall behavior during venous pressure elevation in isolated canine hearts.

We examined the "vascular waterfall" hypothesis, which proposes that coronary flow is unaffected by elevations in outflow pressure until the latter reaches a critical threshold level, in 29 isolated canine hearts. In fibrillating hearts vasodilated with adenosine or carbocromen, coronary flow and the coronary pressure-flow relation were not affected by changes in great cardiac vein pressure (PGCV) below a threshold value of 11 +/- 0.9 (mean +/- SEM) mm Hg. Further elevations of PGCV reduced flow and shifted the pressure-flow relation to the right, increasing its pressure-axis intercept (Pf=0). When vasomotor tone was augmented with vasopressin, threshold PGCV increased to 25 +/- 2.7 mm Hg (p less than 0.001). Once again, the pressure-flow relation was unaffected by changes in PGCV below the threshold value and shifted to the right when this value was exceeded. The amount by which spontaneous values of Pf=0 exceeded threshold values of PGCV was greater when vasomotor tone was augmented than during vasodilation. Pf=0 continued to exceed PGCV when the latter was raised above the threshold level. Both Pf=0 and threshold values of PGCV were less during a long diastole than during ventricular fibrillation. We reached the following conclusions. 1) During changes in PGCV below a threshold value, the coronary circulation exhibits traditional waterfall behavior. 2) The threshold pressure for altering waterfall behavior is affected by vascular tone and mechanical activity. 3) Pf=0 remains above PGCV when the latter is increased above the threshold value needed to alter flow.

Animals↗

PubMed1987

Characterization of capacitance-free pressure-flow relations during single diastoles in dogs using an RC model with pressure-dependent parameters.

Although previous studies have proposed a variety of models to characterize diastolic pressure-flow relations, the models' ability to predict capacitance-free pressure-flow relations from dynamic information in individual studies has not been determined. This study tested the ability of a lumped RC model with pressure-dependent parameters to predict diastolic capacitance-free flow during maximum vasodilation in anesthetized dogs. Model parameters were characterized by perturbing the circumflex coronary artery with a ramp pressure waveform that caused coronary artery pressure to decline at rates varying from 30-150 mm Hg/sec. Capacitance-free relations constructed from declining and rising ramp pressure-flow data corresponded with capacitance-free pressure-flow points constructed during constant-pressure coronary artery perfusion (which are model-independent). The model parameters derived from analysis of the ramp data indicate that conductance of the coronary bed varies directly with coronary pressure and is independent of the rate of coronary pressure decay. Values of coronary capacitance vary inversely with coronary artery pressure and with the magnitude of dPLC/dt. Thus, a simple, lumped diastolic model with pressure-dependent parameters can predict capacitance-free pressure-flow behavior from dynamic pressure-flow data and characterize model parameters over a wide range of coronary pressure.

Adenosine↗

PubMed1985

Pressure and tone dependence of coronary diastolic input impedance and capacitance.

To quantify reactive elements of the coronary circulation, we have characterized in vivo diastolic coronary input impedance by introducing sinusoidal pressure oscillations of constant amplitude and varying frequency at constant mean pressure levels during prolonged diastoles in heart-blocked dogs anesthetized with pentobarbital. The behavior of coronary input impedance is similar to that observed in other peripheral vascular beds and is a function of both mean distending pressure and vasomotor tone. The behavior of impedance modulus and phase at each pressure level could be described by a lumped resistive-capacitive (RC) parallel model over a frequency range of 1-5 Hz. At higher frequencies the phase angle response could be characterized by adding a Voigt viscoelastic element to the original RC model. Calculated coronary capacitances for both models were similar in magnitude and varied inversely with mean coronary distending pressure. Values for the RC and RC viscoelastic model in the maximally dilated coronary bed were 14.1 and 21.6 X 10(-3) ml X mmHg X 100 g-1 at 30 mmHg and 2.65 and 2.70 X 10(-3) ml X mmHg-1 X 100 g-1 at 110 mmHg. With vasomotor tone intact, calculated coronary capacitance at each pressure level was reduced by a factor of two. These results indicate that an RC parallel model with pressure- and vasomotor tone-dependent capacitance adequately describes diastolic coronary input impedance at frequencies encountered during ordinary diastoles. The addition of a viscoelastic element provides adequate fits up to frequencies of 10 Hz.

Animals↗

PubMed1985

Coronary pressure-flow relationships. Controversial issues and probable implications.

On the basis of the material discussed, our current assessments of the controversial points mentioned at the beginning of this article may be summarized as follows: Pf = 0, the minimum back pressure to coronary flow associated with a measurable conductance, is indeed greater than coronary outflow pressure (and usually left ventricular diastolic pressure, as well). Pf = 0 needs to be taken into account in attempts to determine coronary driving pressure. In maximally vasodilated beds, Pf = 0 derived from diastolic pressure-flow relationships exceeds coronary outflow pressure by at least a few mm Hg. Pf = 0 varies with coronary outflow and/or diastolic ventricular cavity pressure. When left ventricular preload is elevated, Pf = 0 exceeds outflow pressure by increasing amounts. Pf = 0 appears to be systematically higher and pressure-dependent in beds in which vasomotor tone is operative. An improved understanding of the nature of, and basis for, time-dependent changes in resistance and/or Pf = 0 during long diastoles in nonvasodilated beds is needed. The contour of pressure-flow relationships which are free of reactive effects is curvilinear rather than linear. The degree of curvilinearity is substantial and can change with interventions. Curvilinearity is accentuated at lower pressures and may reflect changes in the number of perfused vascular channels as well as the caliber of individual channels. Capacitive effects need to be dealt with quantitatively in studies of pressure-flow relationships. Values of the capacitance which is involved in these effects vary with both pressure and tone. Capacitive flow also depends upon the instantaneous rate of change of pressure, which has not usually been defined in published studies. Although intramyocardial capacitance is large and plays an important role in systolic-diastolic flow interactions, a controlling role in diastolic coronary arterial pressure-flow relationships has not been established experimentally. In vasodilated beds, in-flow remains remarkably constant for several seconds after the brief transient associated with a step-change in the level of constant pressure perfusion during a long diastole. Calculations of coronary vascular resistance (by whatever method) remain of limited value, particularly when changes in response to an intervention are modest. Because of the curvilinear diastolic pressure-flow relationship, resistance is pressure-dependent and, at any given pressure, is probably best defined by establishing the slope of a diastolic pressure-flow curve which is free of reactive effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1978

Fluid dynamics of coronary artery stenosis.

A large-scale model of the coronary circulation, instrumented to permit detailed pressure and velocity measurements, has been used to study flow through isolated stenotic elements in large coronary arteries. Pulsatile aortic and instantaneous peripheral resistance were stimulated with servovalves. A variety of axisymmetric and asymmetric stenoses were studied and flow separation was found to occur for all but very mild stenoses. Pressure recovery downstream of the stenosis throat was limited and, in some cases, no recovery was observed. Pressure drop was primarily dependent upon the minimum area of the stenosis and relatively independent of stenosis geometry. Flow was quasi-steady at normal heart rates, and simple steady flow theory proved adequate to describe the pressure drop through the stenosis. The theory yielded results that agreed well with published data for dogs and appears promising for predicting effects of hemodynamic variables on a given stenotic lesion. Thus, principal findings of the study are that a relatively severe stenosis behaves essentially like an orifice and that a simple quasi-steady theory appears adequate to predict effects of a stenosis on coronary flow.

Blood Pressure↗

PubMed1975

Influence of crossbridge compliance on the force-velocity relation of muscle.

It is shown that muscle models which describe force generation as being dependent on the extension of the individual crossbridges produce a force-velocity relation of the form: Vf= Visotonic--1/KHS dP/dt. The derivation of this equation is independent of the details of activation and the kinetics of the crossbridges. The velocity, Vf, represents the relative filament velocity, and Visontonic is the relative filament velocity which would maintain a constant muscle force. P. The quantity KHS is the net stiffness of all the force-generating crossbridges in one-half a sarcomere. Experimental methods for determining KHS are suggested . To study the force-velocity relation, computer simulations based on A. F.Huxley's 1957 kinetic model were conducted for isometric and isotonic twitch contractions. The relative filament velocity is found to depend on the contraction mode, exhibiting a sudden increase in an isometric-to-isontonic changeover and a decrease in the reverse process.

Biomechanical Phenomena↗

PubMed1975

An efficient optimization technique for recovering ventilation-perfusion distributions from inert gas data. Effects of random experimental error.

A variable metric optimization method of numerical analysis has been used to recover known distributions of intrapulmonary ventilation-perfusion ratios from inert gas data. Hypothetical lungs were simulated and corresponding inert gas retentions calculated. By using error-free retentions for seven gases and a 50-compartment model, it was possible to recover distributions containing up to three modes accurately and with greater efficiency than with other numerical methods. When random error of a magnitude consistent with present analytical techniques was introduced into retention data, the recovered distributions differed qualitatively from the original ones. This resulted from the ill-conditioned nature of the mathematical problem, which makes a recovered distribution extremely sensitive to small errors in retention. Thus, present levels of measurement error represent an important limitation in current techniques for deriving distributions from inert gas measurements.

Gases↗

PubMed1974