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R S Aronson

Publications and source records attributed to R S Aronson.

At least 37 records · Page 2Linked to original sources
PubMed1982

Passive electrical properties of normal and hypertrophied rat myocardium.

We determined the electrical constants of epicardial and endocardial preparations from both normal and hypertrophied rat hearts. This was done by comparative analysis of the spatial decay of steady-state electronic voltage deflection produced by injection of a hyperpolarizing constant-current pulse. We used a two-dimensional finite disk model to obtain the apparent membrane resistance, (Rm)app, and internal longitudinal resistivity (Ri), (Rm)app was significantly larger in epicardial (565 +/- 222 omega . cm2) than endocardial (375 +/- 137) preparations from normal hearts. This regional difference disappeared in hypertrophied hearts (epicardium 421 +/- 138, endocardium 383 +/- 121 omega . cm2). Ri was similar for normal endocardial (272 +/- 169 omega . cm) and epicardial (326 +/- 152) preparations, as well as for hypertrophied endocardial (251 +/- 108) and epicardial (312 +/- 59) preparations. We determined the effective membrane capacity (Ceff) by measuring the ratio of applied charge to the displacement of membrane potential. Ceff was larger for normal hearts (epicardium 9.7 +/- 2.5 micro F/cm2, endocardium 7.5 +/- 3.0) than for hypertrophied hearts (epicardium 4.1 +/- 1.4, endocardium 4.7 +/- 1.2). From the values for Ceff we calculated the effective membrane resistance, (Rm)eff. (Rm)eff was larger for normal (epicardium 5,392 +/- 2,613 omega . cm2, endocardium 3,013 +/- 2,096) than for hypertrophied (epicardium 1,552 +/- 633, endocardium 1,838 +/- 826) preparations. Our results show that the amount of electrically effective membrane area is decreased in hypertrophied myocardium, despite the increased total area per hypertrophied cell. One functional implication of this finding is that activation of contraction by spread of surface electrical depolarization into the T-tubules may be impaired in hypertrophied cardiac muscle.

Animals↗
PubMed1982

Reversible alterations in excitation-contraction coupling during myocardial hypertrophy in rat papillary muscle.

To investigate the possible role of an alteration in excitation-contraction coupling in cardiac hypertrophy, we compared simultaneously recorded action potentials along with isometric or isotonic contractions of normal and hypertrophied papillary muscles. Hypertrophy was produced by renal hypertension in rats. Hypertrophied papillary muscles were taken from rats that had been hypertensive for 10 [HBP (10)] or 20 [HBP (20)] weeks. Regression of changes induced by hypertrophy was studied in rats that had been hypertensive for 10 weeks and then made normotensive for 10 weeks by removal of the ischemic kidney. Papillary muscles from age-matched, sham-operated rats [SHAM (10), SHAM (20)] were used as controls. We found that HBP (10) rats had significantly longer action potentials than SHAM (10) rats and that difference in the action potential duration recorded during isotonic and isometric contractions was significantly different from SHAM (10) and HBP (10) rats. Peak developed tension was the same in HBP (10) and SHAM (10) muscles, but the duration of isometric contraction and time-to-peak shortening were longer in HBP (10) muscles. Similarly, whereas the peak tension was the same in HBP (20) and SHAM (20) muscles, the duration of the action potential and isometric contraction, as well as the time-to-peak tension, was longer in HBP (20) muscles. The longer values for action potential duration, isometric contraction, and time-to-peak tension in HBP (20) muscles returned to SHAM values in HBP (R) muscles. The functional relationship between contraction and the action potential time course was assessed by plotting action potential duration against four parameters of contraction: peak developed tension, time-to-peak tension, time-to-half relaxation, and time-to-peak shortening. Statistical analysis of these data showed a significant correlation between action potential duration and all four parameters of contraction in SHAM (10) and SHAM (20) muscles. In contrast, HBP (10) muscles showed a significant correlation between action potential duration and only two contractile parameters, whereas action potential duration did not correlate significantly with any of the contractile parameters in HBP (20) muscles. Remarkably, in HBP (R) preparations a significant correlation was restored between action potential duration and three of the four contractile parameters. The results of this study suggest that reversible cardiac hypertrophy is associated with reversible alterations in excitation-contraction coupling. The reversibility of the mechanical and electrical alterations that accompany hypertrophy suggests, in turn, that cardiac hypertrophy is an adaptive process.

Action Potentials↗
PubMed1981

Transmembrane action potentials and the electrocardiogram in rats with renal hypertension.

The results of previous studies of the relation between the surface electrocardiogram and cellular transmembrane potentials have suggested that the T wave configuration of the ECG is the result of a difference in the duration of endocardial and epicardial action potentials. Ventricular hypertrophy induced by renal hypertension in rats is associated with lengthening of action potential duration and a reproducible decrease in T wave magnitude. Therefore, this model was used to study the relation between the surface T wave configuration and regional differences in action potential duration. ECGs were recorded from hypertensive (HBP) and sham-operated (SHAM) rats. The hearts from these animals were removed and transmembrane action potentials were recorded by standard microelectrode techniques from endocardial and epicardial preparations. We found that the normally peaked T waves seen in the ECG of SHAM rats was reduced by 35% in the ECG of HBP rats. This reduction of T wave magnitude was associated with similar duration of epicardial and endocardial action potentials in HBP rats. However, peaked T wave in SHAM ECG was not accompanied by a significant disparity in the duration of the epicardial and endocardial action potentials. Thus, there is no simple, consistent correlation between surface T wave configuration and regional differences in intracellular action potential duration in rats.

Action Potentials↗
PubMed1981

Afterpotentials and triggered activity in hypertrophied myocardium from rats with renal hypertension.

We have found that afterpotentials can be induced selectively in hypertrophied myocardium from rats with renal hypertension. Three kinds of afterpotentials were recorded by standard microelectrode techniques: early afterdepolarizations, delayed afterdepolarizations, and early afterdepolarizations. The first two kinds of afterpotentials could give rise to triggered spontaneous activity, whereas the last kind did not. Delayed afterdepolarizations were induced in hypertrophied fibers exposed to Tyrode's solution containing high extracellular calcium ([Ca2+]o = 7.2-12 mM) and early afterdepolarizations occurred in hypertrophied fibers exposed to Tyrode's solution containing tetraethylammonium (TEA = 10-30 mM). Neither of these treatments produced afterpotentials in normal myocardium. We found that delayed afterdepolarizations became larger when the stimulation frequency, number of preceding driven beats, or [Ca2+]o was increased. The coupling interval from the upstroke of the last driven action potential to the peak of the delayed afterdepolarization decreased when the stimulation frequency or number of preceding driven beats increased. Hypertrophied fibers treated with high [Ca2+]o that gave rise to triggered activity showed a characteristic relationship between delayed afterpotential magnitude and drive cycle length. In hypertrophied muscles treated with TEA, triggered activity developed from an early afterdepolarizations but terminated with a delayed afterdepolarization. The occurrence of afterpotentials in hypertrophied, but not in normal myocardium, appears to reflect the development of an important electrophysiological alteration that may predispose hypertrophied fibers to develop arrhythmias.

Action Potentials↗
PubMed1981

Non-uniform electrophysiological properties and electrotonic interaction in hypertrophied rat myocardium.

We studied the distribution and nature of the electrical changes associated with myocardial hypertrophy induced by renal hypertension in rats. Standard microelectrode techniques were used to study transmembrane action potentials recorded from endocardial, papillary muscle, and epicardial stimulation from hypertrophied (HBP) and normal (SHAM) hearts. We also determined the effects of stimulation frequency on the action potentials recorded from these preparations. To assess whether altered intercellular electrical connections contribute to the electrophysiological changes associated with hypertrophy, we analyzed the spatial steady state voltage decrement produced by passing intracellular constant current pulses and determined the effective input resistance (Rin) of endocardial HBP and SHAM preparations. Our results show that the action potential prolongation that accompanies hypertrophy is not uniform. Thus, the entire course of repolarization is prolonged in epicardial and papillary muscle fibers, but only the latter half of repolarization is prolonged in epicardial fibers. Endocardial action potentials is general, and HBP action potentials in particular, have a distinctive steep relation between duration and stimulation frequency which may be due to a difference in the rate dependence of a membrane conductance(s), although relatively greater accumulation of extracellular potassium or altered activity of the Na+-K+ pump cannot be excluded as contributing factors. In addition, the similarity in the profile of spatial voltage decrement and the values for Rin in HBP and SHAM preparations indicates that alterations in electrotonic coupling between cells are unlikely to account for the prolonged action potentials of hypertrophied myocardium.

Action Potentials↗
PubMed1977

The effect of ouabain, dinitrophenol, and lithium on the pacemaker current in sheep cardiac Purkinje fibers.

We studied the effect of ouabain and other inhibitors of the Na-K pump on the pacemaker current (IK2) in sheep cardiac Purkinje fibers. We found that exposure to ouabain (2 X 10(7) M) caused an apparent decrease in the amplitude of the IK2 activation curve. We also found that a similar effect was caused by exposure to dinitrophenol (DNP) or lithium-substituted Tyrode's solution. Our studies showed that after prolonged (more than 60 minutes) exposure to ouabain a characteristic current noise appeared and IK2 was replaced by an oscillatory inward current (IOS). The apparent threshold for IOS was -50 to -60 mV and the peak amplitude of this current increased with increasing levels of depolarization positive to threshold. These results suggest that (1) the apparent decrease in IK2 may be a consequence of ionic redistribution due to Na-K pump inhibition; (2) cardiac glycosides cause abnormal impulse generation by an ionic mechanism separate from IK2 and involving IOS.

Animals↗
PubMed1977

Voltage clamp analysis of the effects of dopamine on the transmembrane ionic currents underlying the action potential of sheep cardiac Purkinje fibers.

Dopamine shifted the voltage-dependence of the slow outward current that underlies spontaneous diastolic depolarization to a more positive voltage range and increased the rate constants of inactivation of this current at voltages negative to -80 mV. Dopamine increased the magnitude of the slow inward current and the delayed outward current. Dopamine had an inconsistent effect on the positive dynamic current and the time-independent potassium current. These effects were consistent with effects on the slope of diastolic depolarization, plateau voltage, and action potential duration and are similar to those of epinephrine. The effects of dopamine on the slow inward current and on the delayed outward current were abolished by verapamil, a slow channel blocker. This finding substantiates that outward potassium currents are modulated by intracellular calcium.

Action Potentials↗
PubMed1975

Effect of transmembrane potential on the manifestations of ouabain toxicity in sheep cardiac Purkinje fibres.

The effect of membrane potential on the manifestations of ouabain-induced alterations in the electrical activity of shortened sheep cardiac Purkinje fibres was studied by a microelectrode technique. The level of membrane potential was modulated by passing intracellular polarizing current. It was found that the toxic electrical effects induced by exposure to ouabain vary according to the level of membrane potential.

Animals↗
PubMed1975

A circuit for measuring maximum negative or positive potentials.

A circiut was designed for measuring maximum negative or positive potentials occurring during an action potential. The basic functional unit is a peak-holding circuit that is reset following each action potential. The output of the circuit is displayed on a digital meter and may also be used to drive a point plotter for a graphic presentation of data.

Action Potentials↗
PubMed1973

The electrical activity of canine cardiac Purkinje fibers in sodium-free, calcium-rich solutions.

Propagated action potentials can be obtained in canine cardiac Purkinje fibers exposed to Na-free solutions containing no inorganic cation other than Ca and K. Essentially similar action potentials are obtained if Na is replaced by tetraethylammonium (TEA), tetramethylammonium (TMA), or choline. In a solution containing 128 mM TEA and 16.2 mM Ca the characteristics of these electrical responses were: maximum diastolic potential, -59 +/- 3.3 mV; overshoot, 20 +/- 6.8 mV; maximum upstroke velocity, 3.7 +/- 2.3 V/s; conduction velocity, 0.1 m/s; and action potential duration, 360 +/- 45 ms. The magnitude of the overshoot varied with log Ca(o) with a slope of about 30 mV/10-fold concentration change. The upstroke velocity was an approximately linear function of Ca(o). The active response was greatly diminished or abolished by Mn and D-600 but was unaffected by tetrodotoxin. These Ca-dependent responses appeared in a region of transmembrane potential (about -50 mV) at which the rapid Na-dependent upstroke is abolished even when Na is present.

Action Potentials↗