scholarly journals Active State in Heart Muscle

1967 ◽  
Vol 50 (3) ◽  
pp. 661-676 ◽  
Author(s):  
Edmund H. Sonnenblick
Keyword(s):  
Heart Muscle ◽  
Mechanical Response ◽  
Electrical Stimulus ◽  
Isometric Tension ◽  
Maximum Intensity ◽  
Active State ◽  
Tension Development ◽  
Peak Tension ◽  
Time To Peak ◽  
Time Required

The course of active state in heart muscle has been analyzed using a modified quick release method. The onset of maximum active state was found to be delayed, requiring 110–500 msec from time of stimulation, while the time to peak isometric tension required 250–650 msec. Further, the time from stimulation to peak tension was linearly related to the time required to establish maximum intensity of active state as well as to the duration of maximum active state. The duration of maximum active state was prolonged (90–220 msec), occupying most of the latter half of the rising phase of the isometric contraction. Norepinephrine (10-5 M) shortened the latency from electrical stimulus to mechanical response, accelerated the onset of maximum active state, increased its intensity, decreased its duration, and accelerated its rate of decline. These changes were accompanied by an increase in the rate of tension development and the tension developed while the time from stimulation to peak isometric tension was abbreviated. Similar findings were shown for strophanthidin (1 µg/ml) although lesser decrements in the duration of maximum active state and time to peak tension were found than with norepinephrine for similar increments in the maximum intensity of active state.

Effect of hypoxia on mechanical function in the neonatal mammalian heart

1978 ◽  
Vol 235 (5) ◽  
pp. H469-H474 ◽  
Author(s):  
J. M. Jarmakani ◽  
M. Nakazawa ◽  
T. Nagatomo ◽  
G. A. Langer
Keyword(s):  
Glycolytic Pathway ◽  
Mechanical Function ◽  
Maximal Rate ◽  
Half Time ◽  
Perfusion Rate ◽  
Tension Development ◽  
Peak Tension ◽  
Time To Peak ◽  
Newborn Rabbit ◽  
Mammalian Heart

The effect of 30 min of hypoxia followed by reoxygenation on mechanical function was studied in isolated, arterially perfused, neonatal rabbit and dog hearts. All studies were performed at a perfusion rate of 2.5 ml/g-min, at a pacing rate of 60 beats/min and at 27 degrees C. The muscles were perfused with Krebs-Henseleit solutions equilibrated with 95% O2 and 5% CO2 (control) or 95% N2 and 5% CO2 (hypoxia). In the newborn rabbit and dog, both the developed tension (DT) and the maximal rate of tension development (dT/dtmax+) decreased during the first 3 min of hypoxia and then recovered to values not different from control. The effect of hypoxia on DT and dT/dtmax+ was inversely related to age in both the rabbit and dog. The equations describing the decline in DT and dT/dTmax+ during hypoxia and the recovery during reoxygenation were best expressed by two or three exponentials. Time to peak tension and half time to relaxation decreased during hypoxia and the decrease was also inversely related to age. The fact that the newborn was able to maintain normal mechanical function during hypoxia suggests that the newborn is capable of maintaining normal myocardial ATP levels due to enhanced flux through the glycolytic pathway.

Enhanced contractility during relaxation of cat papillary muscle

1975 ◽  
Vol 228 (6) ◽  
pp. 1708-1716 ◽  
Author(s):  
BG Bass
Keyword(s):  
Papillary Muscle ◽  
Time Course ◽  
Isometric Tension ◽  
Contractile Element ◽  
Cat Papillary Muscle ◽  
Postextrasystolic Potentiation ◽  
Peak Tension ◽  
Time To Peak ◽  
In Series ◽  
Antecedent Control

Contractility during relaxation of isometric tension was studied in isolated, electrically driven cat papillary muscle by interpolation of test extrasystoles, all of whichpartially fused with their antecedent (control) contractions, were separated by computer from the fused contractions and then analyzed. The time course of the restitutionof contractility during relaxation was defined by plotting maximal positive dT/dt andtime-to-peak tension of the computer-separated extrasystole versus delay preceding the extrasystole. The dT/dt and time-to-peak tension, which steadily decline with progressive prematurity between contractions, both increase again during late relaxation, become progressively greater still earlier in relaxation, peak shortly after peak isometric tension, and then again decline. This phase of an apparently enhanced contractilityduring relaxation is depressed in low Ca'++ and is transmitted into the postextrasystolic period (in which it is superimposed on the usual postextrasystolic potentiation). The possible contributions of variations in series-elastic component and contractile-element lengths, actionpotential characteristics, and other factors on contractility during relaxation are discussed. It is suggested that enhanced contractility during relaxation may also be related in part to the decay of the intracellular free Ca'++ transient.

scholarly journals The O2 cost of the tension-time integral in isolated single myocytes during fatigue

2010 ◽  
Vol 298 (4) ◽  
pp. R983-R988 ◽  
Author(s):  
Russell T. Hepple ◽  
Richard A. Howlett ◽  
Casey A. Kindig ◽  
Creed M. Stary ◽  
Michael C. Hogan
Keyword(s):  
Slow Component ◽  
Motor Units ◽  
Isometric Tension ◽  
Aerobic Metabolism ◽  
Whole Body ◽  
Cellular Respiration ◽  
Tension Development ◽  
Phosphorescence Quenching ◽  
Contraction Frequency ◽  
Peak Tension

One proposed explanation for the V̇o2 slow component is that lower-threshold motor units may fatigue and develop little or no tension but continue to use O2, thereby resulting in a dissociation of cellular respiration from force generation. The present study used intact isolated single myocytes with differing fatigue resistance profiles to investigate the relationship between fatigue, tension development, and aerobic metabolism. Single Xenopus skeletal muscle myofibers were allocated to a fast-fatiguing (FF) or a slow-fatiguing (SF) group, based on the contraction frequency required to elicit a fall in tension to 60% of peak. Phosphorescence quenching of a porphyrin compound was used to determine Δ intracellular Po2 (PiO2; a proxy for V̇o2), and developed isometric tension was monitored to allow calculation of the time-integrated tension (TxT). Although peak ΔPiO2 was not different between groups ( P = 0.36), peak tension was lower ( P < 0.05) in SF vs. FF (1.97 ± 0. 17 V vs. 2. 73 ± 0.30 V, respectively) and time to 60% of peak tension was significantly longer in SF vs. FF (242 ± 10 s vs. 203 ± 10 s, respectively). Before fatigue, both ΔPiO2 and TxT rose proportionally with contraction frequency in SF and FF, resulting in ΔPiO2/TxT being identical between groups. At fatigue, TxT fell dramatically in both groups, but ΔPiO2 decreased proportionately only in the FF group, resulting in an increase in ΔPiO2/TxT in the SF group relative to the prefatigue condition. These data show that more fatigue-resistant fibers maintain aerobic metabolism as they fatigue, resulting in an increased O2 cost of contractions that could contribute to the V̇o2 slow component seen in whole body exercise.

Chronic verapamil treatment attenuates the negative inotropic effect of ethanol in diabetic rat myocardium

1994 ◽  
Vol 72 (9) ◽  
pp. 1013-1018 ◽  
Author(s):  
Ricardo A. Brown ◽  
Prashant Bhasin ◽  
Adedapo O. Savage ◽  
Joseph C. Dunbar
Keyword(s):  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Diabetic Rat ◽  
Tension Development ◽  
Altered Expression ◽  
Peak Tension ◽  
Time To Peak ◽  
Diabetic Myocardium

It is well established that cardiomyopathy is a consistent feature of diabetic myocardium and that alcohol consumption increases the risk of cardiovascular disease among diabetic subjects. The objective of this investigation was to determine whether acute or chronic verapamil treatment attenuates the negative inotropic effect of ethanol (EtOH) in the diabetic rat heart. Wistar rats were made diabetic with streptozotocin (55 mg/kg, iv). Left-ventricular papillary muscles, from normal and diabetic (8 weeks) rats, were superfused with Tyrode's solution at 30 °C while driven at 0.5 Hz. A subgroup of diabetic and normal animals received daily injections of verapamil (8 mg/kg, ip; 8 weeks), whereas muscles from untreated animals were exposed to verapamil (2 μM) in vitro. Peak tension developed (PTD), time to peak tension (TPT), time to 90% relaxation (RT90), and the maximum velocities of tension development (+VT) and decay (−VT) were determined in the absence and presence of clinically relevant concentrations of EtOH (80–240 mg/dL, i.e., 17.4–52.1 mM). Ethanol at 80 mg/dL reduced PTD, + VT, and −VT only in preparations from diabetic animals. Higher concentrations of EtOH (120–240 mg/dL) decreased PTD, TPT, +VT, and −VT. The negative inotropic effect of EtOH (240 mg/dL) was attenuated only in diabetic myocardium chronically treated with verapamil, whereas acute verapamil treatment potentiated the negative inotropic effect of EtOH in both normal and diabetic myocardium. Thus, chronic verapamil therapy diminishes the negative inotropic effect of EtOH in diabetic myocardium and acute verapamil treatment exaggerates it. Altered expression of membrane-bound calcium channels may be involved in the negative inotropic response to EtOH in long-term diabetes.Key words: ethanol, papillary muscle, inotropism, myocardium, force of contraction, diabetes mellitus.

scholarly journals Timing and magnitude of systolic stretch affect myofilament activation and mechanical work

2014 ◽  
Vol 307 (3) ◽  
pp. H353-H360 ◽  
Author(s):  
Jared R. Tangney ◽  
Stuart G. Campbell ◽  
Andrew D. McCulloch ◽  
Jeffrey H. Omens
Keyword(s):  
Force Transducer ◽  
Isometric Tension ◽  
Mechanical Work ◽  
In Vivo Studies ◽  
Time Varying ◽  
Force Output ◽  
External Work ◽  
Tension Development ◽  
Peak Tension

Dyssynchronous activation of the heart leads to abnormal regional systolic stretch. In vivo studies have suggested that the timing of systolic stretch can affect regional tension and external work development. In the present study, we measured the direct effects of systolic stretch timing on the magnitude of tension and external work development in isolated murine right ventricular papillary muscles. A servomotor was used to impose precisely timed stretches relative to electrical activation while a force transducer measured force output and strain was monitored using a charge-couple device camera and topical markers. Stretches taking place during peak intracellular Ca2+ statistically increased peak tension up to 270%, whereas external work due to stretches in this interval reached values of 500 J/m. An experimental analysis showed that time-varying elastance overestimated peak tension by 100% for stretches occurring after peak isometric tension. The addition of the force-velocity relation explained some effects of stretches occurring before the peak of the Ca2+ transient but had no effect in later stretches. An estimate of transient deactivation was measured by performing quick stretches to dissociate cross-bridges. The timing of transient deactivation explained the remaining differences between the model and experiment. These results suggest that stretch near the start of cardiac tension development substantially increases twitch tension and mechanical work production, whereas late stretches decrease external work. While the increased work can mostly be explained by the time-varying elastance of cardiac muscle, the decreased work in muscles stretched after the peak of the Ca2+ transient is largely due to myofilament deactivation.

scholarly journals The Effects of Temperature upon Contraction and Ionic Exchange in Rabbit Ventricular Myocardium

1968 ◽  
Vol 52 (4) ◽  
pp. 682-713 ◽  
Author(s):  
G. A. Langer ◽  
A. J. Brady
Keyword(s):  
Ventricular Myocardium ◽  
Isometric Tension ◽  
Active State ◽  
Ionic Exchange ◽  
Active Tension ◽  
Tension Development ◽  
Mechanical Responses ◽  
Abrupt Changes ◽  
Rabbit Ventricular Myocardium ◽  
Temperature Rate

The mechanical responses (active and resting tension, dP/dt, TPT) and ionic exchange characteristics (Ca++, K+, Na+) which follow upon a variation in temperature, rate, and [K+]0 were studied in the rabbit papillary muscle and arterially perfused rabbit interventricular setpum. Abrupt changes in temperature provided a means of separating the contributions of rate of development (intensity) of active state and duration of active state to total active tension development (approximated by isometric tension). Threefold changes in duration of active state with proportional changes in active tension can be induced without evidence for alteration of Ca++, K+, or Na+ exchange. Abrupt cooling produced a moderate (∼15%) increase of dP/dt which suggests an augmentation of active state intensity. Evidence is presented to suggest that this increase of dP/dt is based upon an increase in membrane Ca++ concentration which occurs secondary to inhibition of active Na+ transport. The alterations in ionic exchange and active state produced by variation of temperature are discussed in terms of a five-component control system.

Influence of poststimulation potentiation and heart rate on the fetal lamb heart

1975 ◽  
Vol 229 (2) ◽  
pp. 318-323 ◽  
Author(s):  
SE Kirkpatrick ◽  
J Naliboff ◽  
PT Pitlick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Recovery Period ◽  
Control Level ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Atrial Pacing ◽  
Tension Development ◽  
Time To Peak ◽  
Fetal Lamb

Isolated cardiac muscle techniques and studies of the chronically instrumented fetal lamb heart were employed to evaluate the ability of fetal myocardium to exhibit poststimulation potentiation. Isometric tension development and the response to paired electrical stimulation were significantly reduced in isolated fetal ventricular myocardium when compared to the adult (P less than 0.001). As in the adult, increasing stimulation frequency raised fetal isometric tension via an increase in the rate of rise of tension development in the presence of reduction in time-to-peak tension. In seven fetal lambs the left ventricle was chronically instrumented with endocardial ultrasonic crystals and a high-fidelity micromanometer. After a 2-wk recovery period, heart rate was increased by atrial pacing from an average control level of 150 to 300 beats/min. Left ventricular dP/dt increased progressively and then fell beyond a heart rate of 270/min. When comparable pre- and immediate postpacing beats were analyzed, a step-wise increase in the velocity of left ventricular shortening and the mean rate of circumferential fiber shortening was observed in association with an increase in the extent of shortening. Thus, increases in the frequency of contraction exert a significant positive inotropic effect on the fetal heart.

Calcium fluxes and contractility in isolated guinea pig atrium: effect of A23187

1978 ◽  
Vol 235 (1) ◽  
pp. C13-C19 ◽  
Author(s):  
D. R. Holland ◽  
W. M. Armstrong ◽  
M. I. Steinberg
Keyword(s):  
Guinea Pig ◽  
Myocardial Cell ◽  
Ionophore A23187 ◽  
Inotropic Action ◽  
Tension Development ◽  
Peak Tension ◽  
Time To Peak ◽  
Endogenous Histamine ◽  
Resultant Increase ◽  
45Ca Efflux

The Ca2+ ionophore A23187 (10(-6) to 3 X 10(-5) M) increased the force of contraction is isolated guinea pig atria. In individual twitches, peak tension, maximum rate of tension development, time to peak tension, and total twitch duration were all increased by A23187. Tripelennamine, indomethacin, and atropine did not significantly alter the inotropic effect of A23187. Serotonin produced changes in individual twitches that differed qualitatively and quantitatively from those of A23187. Therefore, the inotropic action of A23187 is probably not mediated by release of endogenous histamine, prostaglandins, acetylcholine, or serotonin. 45Ca influx and efflux were increased by A23187. The enhanced 45Ca efflux exceeded that which would be predicted if the ionophore acted only to increase the passive Ca2+ permeability of the myocardial cell membrane. These results suggest that A23187 facilitates the entry of extracellular Ca2+ into the myocardial cell and the release of intracellular Ca2+ stores into the myoplasm. The resultant increase in intracellular Ca2+ activity could account for the positive inotropic action of A23187.

scholarly journals Depolarization-contraction coupling in short frog muscle fibers. A voltage clamp study.

1984 ◽  
Vol 84 (1) ◽  
pp. 133-154 ◽  
Author(s):  
C Caputo ◽  
F Bezanilla ◽  
P Horowicz
Keyword(s):  
Muscle Fibers ◽  
Tension Development ◽  
Contraction Coupling ◽  
Maximum Tension ◽  
Peak Tension ◽  
Relaxation Phase ◽  
Time To Peak ◽  
Intracellular Ca ◽  
Charge Movements ◽  
Internal Potential

Short muscle fibers (1.5 mm) were dissected from hindlimb muscles of frogs and voltage clamped with two microelectrodes to study phenomena related to depolarization-contraction coupling. Isometric myograms obtained in response to depolarizing pulses of durations between 10 and 500 ms and amplitudes up to 140 mV had the following properties. For suprathreshold pulses of fixed duration (in the range of 20-100 ms), the peak tension achieved, the time to peak tension, and contraction duration increased as the internal potential was made progressively more positive. Peak tension eventually saturates with increasing internal potentials. For pulse durations of greater than or equal to 50 ms, the rate of tension development becomes constant for increasing internal potentials when peak tensions become greater than one-third of the maximum tension possible. Both threshold and maximum steepness of the relation between internal potential and peak tension depend on pulse duration. The relation between the tension-time integral and the stimulus amplitude-duration product was examined. The utility of this relation for excitation-contraction studies is based on the observation that once a depolarizing pulse configuration has elicited maximum tension, further increases in either stimulus duration or amplitude only prolong the contractile response, while the major portion of the relaxation phase after the end of a pulse is exponential, with a time constant that is not significantly affected by either the amplitude or the duration of the pulse. Hence, the area under the tension-response curve provides a measure of the availability to troponin of the calcium released from the sarcoplasmic reticulum in response to membrane depolarization. The results from this work complement those obtained in experiments in which intramembrane charge movements related to contractile activation were studied and those in which intracellular Ca++ transients were measured.

Influence of aldosterone on isometric tension development in the rat heart

1963 ◽  
Vol 204 (6) ◽  
pp. 1001-1004 ◽  
Author(s):  
William C. Ullrick ◽  
Robert L. Hazelwood
Keyword(s):  
Heart Muscle ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Isometric Tension ◽  
Muscle Performance ◽  
Tension Development ◽  
Tension Time ◽  
Isometric Twitch

Isometric twitch curves were recorded from preparations of rat heart trabeculae carneae removed from normal or adrenalectomized animals, or from normal animals injected for 3 days with saline or with 3 µg/day of d-aldosterone. Preparations from normal and from adrenalectomized animals were stimulated for 60 min in aldosterone-free Ringer's solution, or for 30 min in aldosterone-free Ringer's followed by 30 min in Ringer's containing 3 x 10–4 µg/ml of d-aldosterone. For a number of preparations from adrenalectomized animals the concentration of aldosterone was increased to 3 x 10–1 µg/ml. Regardless of treatment, all preparations were stimulated for a total of 1 hr at a rate of approximately 395/min; subsequently the recorded twitch curves were analyzed for peak tension development and for tension-time area. Although adrenalectomy tended to lower these variables of in vitro heart muscle performance, aldosterone, either administered in vivo or added directly to the isolated muscle bath, was without influence. It is concluded that aldosterone in the concentrations used does not alter the isometric tension characteristics of isolated rat heart muscle.

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