Effect of rate changes on strength and time course of contraction of papillary muscle

1963 ◽  
Vol 204 (3) ◽  
pp. 451-457 ◽  
Author(s):  
Jan Koch-Weser
Keyword(s):  
Entire Range ◽  
Maximum Rate ◽  
Time Course ◽  
Normal Development ◽  
Papillary Muscles ◽  
Ventricular Muscle ◽  
High Frequencies ◽  
Peak Tension ◽  
Time To Peak ◽  
Opposing Effect

The influence of 14 frequencies of contraction (between 0.2 and 300 beats/min) on the development of tension and on the time course of contraction was determined in 40 isometrically contracting, isolated cat papillary muscles at 38 C. Only cylindrical muscles with radius <0.43 mm were included, since this was found to be the maximum thickness compatible with normal development of tension at high frequencies. Increases in frequency were associated over the entire range with decreases in the time to peak tension (total 40%) and in the relaxation time (total 49%), and increases in the maximum rate of development of tension (total 560%) and in the peak tension developed (total 340%). These findings indicate that changes in heart rate alter both the degree of activation of the contractile elements and the duration of their active state. It is concluded that the opposing effect of both of these changes must be considered in any analysis of the influence of alterations in rate or rhythm of the heart on the strength of contraction of mammalian ventricular muscle.

Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats

1996 ◽  
Vol 81 (4) ◽  
pp. 1488-1494 ◽  
Author(s):  
George E. Taffet ◽  
Lloyd A. Michael ◽  
Charlotte A. Tate
Keyword(s):  
Exercise Training ◽  
Maximum Rate ◽  
Left Ventricular ◽  
Male Rats ◽  
Papillary Muscles ◽  
Inotropic Response ◽  
Aged Rats ◽  
Adrenergic Stimulation ◽  
Peak Tension ◽  
Time To Peak

Taffet, George E., Lloyd A. Michael, and Charlotte A. Tate.Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats. J. Appl. Physiol. 81(4): 1488–1494, 1996.—Aging is associated with a decreased cardiac responsiveness to β-adrenergic stimulation. We examined the effect of endurance exercise training of old Fischer 344 male rats on β-adrenergic stimulation of the function of isolated left ventricular papillary muscle. Three groups were examined: sedentary mature (SM; 12-mo old), sedentary old (SO; 23–24 mo old), and exercised old (EO; 23–24 mo old) that were treadmill trained for 4–8 wk. The isometric contractile properties were studied at 0.2 Hz and 0.75 mM calcium. Without β-adrenergic stimulation, there were no group differences for peak tension, maximum rate of tension development (+dP/d t), or maximum rate of tension dissipation (−dP/d t). The time to peak tension was longer ( P < 0.05) for both EO and SO than for SM rats. Half relaxation time (RT1/2) was prolonged ( P < 0.05) for SO compared with SM and EO (which did not differ). The three groups did not differ in the β-adrenergic stimulation by isoproterenol of peak tension, −dP/d t, time to peak tension, or contraction duration. The inotropic response (+dP/d t) of SM was greater ( P < 0.05) than that in SO or EO rats (which did not differ); however, the lusitropic response (RT1/2) was lesser ( P < 0.05) in SO than in SM or EO rats (which did not differ). Thus exercise training of old rats improved the lusitropic response to isoproterenol without altering the age-associated impairment in inotropic response.

Inhibition by theophylline of the early component of canine ventricular contraction

1982 ◽  
Vol 242 (3) ◽  
pp. H349-H358
Author(s):  
M. Endoh ◽  
T. Iijima ◽  
S. Motomura
Keyword(s):  
Mechanical Characteristics ◽  
Calcium Influx ◽  
Myocardial Cell ◽  
Ventricular Muscle ◽  
Late Component ◽  
Ventricular Contraction ◽  
Early Component ◽  
Peak Tension ◽  
Time To Peak ◽  
Plateau Potential

Changes in mechanical characteristics of the isolated canine ventricular muscle were investigated during interaction of isoproterenol with theophylline or caffeine. An early and a late component with time to peak tension of 80 and 150 ms, respectively, were differentiated in a single contraction of the muscle stimulated at 0.5 Hz at 37 degrees C during the interaction of isoproterenol and theophylline, or isoproterenol and caffeine. Isoproterenol increased preferentially the early component and affected only slightly the late one. Theophylline or caffeine elevated the early component less than the late one. In the presence of theophylline + isoproterenol or caffeine + isoproterenol the peak tension was achieved by a late component, whereas the increase in the early one induced by isoproterenol in 3 X 10(-7) M and higher was depressed significantly. During the interaction the rate of twitch relaxation was accelerated further rather than depressed. Changes in action potential indicate that the calcium influx via the myocardial cell membrane during depolarization was increased: the peak plateau potential was significantly elevated by theophylline alone and further by theophylline + isoproterenol. These results indicate that theophylline and caffeine (2 mM) may act intracellularly to inhibit the isoproterenol-induced promotion of the early component without impairing the isoproterenol-induced acceleration of relaxation in the canine ventricular muscle.

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.

Effects of pimobendan, a novel inotropic agent, on intracellular calcium and tension in isolated ferret ventricular muscle

1989 ◽  
Vol 76 (6) ◽  
pp. 609-618 ◽  
Author(s):  
J. A. Lee ◽  
J. C. Ruegg ◽  
D. G. Allen
Keyword(s):  
Time Course ◽  
Positive Inotropic Effect ◽  
Inotropic Agent ◽  
Inotropic Effect ◽  
Inhibiting Activity ◽  
Papillary Muscles ◽  
Ventricular Muscle ◽  
Similar Time ◽  
Apparent Increase ◽  
Intact Muscle

1. In this study we have investigated the effects of a novel inotropic agent, pimobendan (UDCG 115-BS), on skinned and intact ventricular muscle from ferrets. 2. Pimobendan (20 or 100 μmol/l) increased tension at a given free [Ca2+] when applied to skinned ventricular muscle, i.e. it increased the Ca2+ sensitivity of the myofibrils. 3. Tension and intracellular free Ca2+ ([Ca2+]i) were measured simultaneously in intact papillary muscles using the aequorin technique. When 25 μmol/l pimobendan was added to the superfusing solution, a slowly developing positive ionotropic effect was produced, which was accompanied by an increase in the size of the systolic rise in [Ca2+]i (Ca2+ transients) with a similar time course. 4. In order to determine whether pimobendan increased the Ca2+ sensitivity of myofibrils in an intact papillary muscle, we compared the increase in Ca2+ transients and tension observed in response to changes in extracellular [Ca2+] with those observed in response to pimobendan. The result of this comparison was that in intact muscle pimobendan caused no apparent increase in myofibrillar Ca2+ sensitivity. 5. Pimobendan caused an abbreviation of the time course of the Ca2+ transients, but the twitch was slightly prolonged. 6. When isoprenaline was added to the superfusing solution, a positive inotropic effect was produced, which was accompanied by a marked increase in the size of the Ca2+ transients. Isoprenaline caused an abbreviation of the time course of both the Ca2+ transients and the twitch. When the Ca2+ sensitivity of the intact myofibrils was determined as described above, isoprenaline caused a desensitization. Pimobendan produced a sensitization when compared with isoprenaline. 7. These results are consistent with the hypothesis that pimobendan produces an inotropic effect in isolated cardiac muscle which is mediated both by an increase in Ca2+ sensitivity and by an increase in adenosine 3′: 5′-cyclic monophosphate due to its phosphodiesterase-inhibiting activity. Such a combination of activities may be particularly advantageous for an inotropic agent.

scholarly journals Sodium and calcium currents in dispersed mammalian septal neurons.

1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Calcium Currents ◽  
Closing Time ◽  
Patch Clamp Technique ◽  
Average Value ◽  
Time To Peak ◽  
Time Courses ◽  
Fast Activation ◽  
Septal Neurons

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.

Characteristics of the second inward current in cells isolated from rat ventricular muscle

1983 ◽  
Vol 219 (1217) ◽  
pp. 447-469 ◽  
Keyword(s):  
Single Cells ◽  
External Solution ◽  
Maximum Level ◽  
Charge Carriers ◽  
Ventricular Muscle ◽  
Inward Current ◽  
Adult Rat ◽  
Time To Peak ◽  
Rat Hearts ◽  
Steady Level

The second inward current ( I si ) in single cells isolated from ventricular muscle of adult rat hearts was measured in response to step depolarizations under voltage-clamp conditions. The major ion carrying this current was Ca, and I si was reduced or abolished by Mn, Ni, Cd, nifedipine, nimodipine and D600. Sr and Ba could substitute for Ca as charge carriers, and reduced the rate of apparent inactivation of I si . These effects of Sr and Ba, together with the relation between the steady level of apparent inactivation and membrane potential in Ca containing solution, were taken as evidence that inactivation was at least in part dependent on internal Ca. The reduction of external Na to 11% of normal caused a reduction in peak I si when Ca was present in the external solution, but did not reduce I si when Ca was replaced by Sr. It therefore seems unlikely that Na is a major charge carrier I si under the conditions of our experiments. The time-to-peak and rate of apparent inactivation of I si were faster than in previous studies that used multicellular preparations. Both the kinetics and peak amplitude of I si were markedly dependent on temperature ( Q 10 close to 3). Contraction of the cells, which was monitored optically, was initiated within 3 ms of the peak I si , reached a maximum level after approximately 40–50 ms, and was about 100 ms in duration.

Abnormal contraction caused by expression of Gi-coupled receptor in transgenic model of dilated cardiomyopathy

2001 ◽  
Vol 280 (4) ◽  
pp. H1653-H1659 ◽  
Author(s):  
Anthony J. Baker ◽  
Charles H. Redfern ◽  
Mark D. Harwood ◽  
Paul C. Simpson ◽  
Bruce R. Conklin
Keyword(s):  
Transgenic Mice ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Myocardial Function ◽  
Expression System ◽  
Contractile Force ◽  
Ventricular Muscle ◽  
Time To Peak ◽  
Contraction And Relaxation

Although increased Gi signaling has been associated with dilated cardiomyopathy in humans, its role is not clear. Our goal was to determine the effects of chronically increased Gi signaling on myocardial function. We studied transgenic mice that expressed a Gi-coupled receptor (Ro1) that was targeted to the heart and regulated by a tetracycline-controlled expression system. Ro1 expression for 8 wk resulted in abnormal contractions of right ventricular muscle strips in vitro. Ro1 expression reduced myocardial force by >60% (from 35 ± 3 to 13 ± 2 mN/mm2, P < 0.001). Nevertheless, sensitivity to extracellular Ca2+ was enhanced. The extracellular [Ca2+] resulting in half-maximal force was lower with Ro1 expression compared with control (0.41 ± 0.05 vs. 0.88 ± 0.05 mM, P < 0.001). Ro1 expression slowed both contraction and relaxation kinetics, increasing the twitch time to peak (143 ± 6 vs. 100 ± 4 ms in control, P < 0.001) and the time to half relaxation (124 ± 6 vs. 75 ± 6 ms in control, P < 0.001). Increased pacing frequency increased contractile force threefold in control myocardium ( P < 0.001) but caused no increase of force in Ro1-expressing myocardium. When stimulation was interrupted with rests, postrest force increased in control myocardium, but there was postrest decay of force in Ro1-expressing myocardium. These results suggest that defects in contractility mediated by Gi signaling may contribute to the development of dilated cardiomyopathy.

Force measurements from voltage-clamped guinea pig ventricular myocytes

1990 ◽  
Vol 258 (2) ◽  
pp. H452-H459 ◽  
Author(s):  
N. Shepherd ◽  
M. Vornanen ◽  
G. Isenberg
Keyword(s):  
Guinea Pig ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Isometric Force ◽  
Contractile Force ◽  
Patch Clamp Technique ◽  
Thin Glass ◽  
Tonic Component ◽  
Time To Peak ◽  
Whole Cell Patch Clamp

We describe the first observations of isolated mammalian guinea pig ventricular myocytes that combine measurements of contractile force with the voltage-clamp method. The myocytes were attached by poly-L-lysine to the beveled ends of a pair of thin glass rods having a compliance of 0.76 m/N. The contractile force of a cell caused a 1- to 3-microm displacement of the rods; the motion of which was converted to an output voltage by phototransistors. By the use of the whole cell patch-clamp technique, the cells were depolarized at 1 Hz with 200-ms-long clamp pulses from -45 to +5 mV (35 degrees C, 3.6 mM CaCl2). Isometric force began after a latency of 7 +/- 2 ms, peaked at 93 +/- 21 ms, and relaxed (90%) at 235 +/- 63 ms. The time course of force was always faster than that of isotonic shortening (time to peak 154 +/- 18 ms). With 400-ms-long depolarizations, a tonic component was recorded as either sustained force or sustained shortening that decayed on repolarization. Substitution of Ca by Sr in the bath increased the inward current through Ca channels but slowed down the time course of force development. The results are consistent with the hypothesis that activator calcium derives mainly from internal stores and that Ca release needs Ca entry through channels.

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.

Sign in / Sign up

Export Citation Format

Share Document