scholarly journals Logistic Time Constant of Isometric Relaxation Force Curve of Ferret Ventricular Papillary Muscle. Reliable Index of Lusitropism.

2000 ◽  
Vol 50 (5) ◽  
pp. 479-487 ◽  
Author(s):  
Ju Mizuno ◽  
Junichi Araki ◽  
Takeshi Mikane ◽  
Satoshi Mohri ◽  
Takeshi Imaoka ◽  
...  
2006 ◽  
Vol 23 (Supplement 37) ◽  
pp. 61
Author(s):  
J. Mizuno ◽  
M. Otsuji ◽  
K. Takeda ◽  
Y. Yamada ◽  
H. Arita ◽  
...  

1989 ◽  
Vol 67 (1) ◽  
pp. 40-46 ◽  
Author(s):  
Paul B. Taylor ◽  
Reinhard K. Helbing ◽  
Sean Rourke ◽  
Dennis Churchill

Cardiac hypertrophy was induced in adult female Wistar rats following 12 days of daily subcutaneous injections of isoproterenol (ISO). The left atria responded with a 13–14% increase in tissue growth, while the ventricles achieved a 34–39% increased tissue mass. Maximum force generation and twitch characteristics in 1.0 mM external Ca2+ for the left atria or the right papillary muscle were unchanged in the ISO-treated animals. The force–interval relation was determined at 26 °C between 0.5 and 120 s. The development of maximum force clearly passed through two phases identified as alpha and beta. To characterize these two processes the data were fitted to a two-term linear combination of exponentials (two-compartment model). The time constant and capacity of each process to contribute to the whole force–interval curve was determined by a four-parameter least square fit method. In control atrial muscle the time constants for the alpha and beta processes were 0.47 and 11.23 s, respectively. The contribution of each process to the total force curve in control atrial muscle was approximately 50% alpha and 50% beta. Following ISO-induced growth the time constants were 0.38 and 13.33 s with a shift of contributions towards 60% alpha and 40% beta. Control papillary muscle from the right ventricle had a similar alpha time constant of 0.49 s compared with atrial muscle but possessed a considerably slower beta time constant of 26.17 s. The contribution of each process to interval-dependent force development was 44.5 and 55.5%, respectively. Treatment with ISO to induce ventricular growth resulted in a 20% reduced alpha time constant, with a 45% increased contribution by the alpha process. These results suggest that during the development of catecholamine-induced hypertrophy, there is a significant change in the fundamental alpha process which appears to be mediated by a reduced time constant and an enhanced capacity to contribute to force development.Key words: excitation–contraction, interval-dependent force recovery, post-rest contractions, cardiac muscle, sarcoplasmic reticulum.


1999 ◽  
Vol 49 (2) ◽  
pp. 145-158 ◽  
Author(s):  
Ju MIZUNO ◽  
Takeshi MIKANE ◽  
Junichi ARAKI ◽  
Mineko HATASHIMA ◽  
Toshiyuki MORITAN ◽  
...  

2007 ◽  
Vol 48 (2) ◽  
pp. 215-232 ◽  
Author(s):  
Ju Mizuno ◽  
Mikiya Otsuji ◽  
Kenji Takeda ◽  
Yoshitsugu Yamada ◽  
Hideko Arita ◽  
...  

1990 ◽  
Vol 259 (5) ◽  
pp. H1601-H1605 ◽  
Author(s):  
F. Mast ◽  
R. C. Woledge ◽  
G. Elzinga

Recovery heat production after contraction in rabbit papillary muscle at 20 degrees C occurs at an exponentially declining rate. The time constant describing this decline is 25 s; it is not different when 10 twitches or when a steady-state twitch train is studied, and it is unaltered by changing stimulus frequency from 0.125 to 0.2 Hz. The same value has previously been found after single twitches. If it is assumed that phosphocreatine (PCr) resynthesis is the cause of recovery heat production and that it occurs also during contractions at a rate proportional to the amount of PCr depletion, it is possible to divide the total heat production for any period of stimulation into that caused by this recovery process (R) and that caused by initial (I) processes (presumed to be PCr splitting). The value of R/I obtained by using this method is 1.10 +/- 0.04 (means +/- SE, n = 27 muscles), close to the theoretical value of 1.13. The correspondence between the measured and the predicted ratio supports the assumptions underlying the measurement. Thus in heart muscle the heat produced during and after contraction can be explained by PCr splitting and reformation. The older Bugnard method of analysis applied to the same data gives an R/I value of 1.5; the reasons for the discrepancy are described.


1969 ◽  
Vol 54 (6) ◽  
pp. 765-781 ◽  
Author(s):  
Yasuzi Sakamoto

Passive and active responses to intracellular and extracellular stimulation were studied in the canine papillary muscle. The electrotonic potential produced by extracellular polarization with the partition chamber method fitted the time course and the spatial decay expected from the cable theory (the time constant, 3.3 msec; the space constant, 1.2 mm). Contrariwise, spatial decay of the electrotonic potentials produced by intracellular polarization was very short and did not fit the decay curve expected for a simple cable, although only a small difference of time course in the electrotonic potentials produced by intracellular and extracellular polarizations was observed. A similar time course might result from the fact that when current flow results from intracellular polarization, the input resistance is less dependent on the membrane resistance. The foot of the propagated action potential rose exponentially with a time constant of 1.1 msec and a conduction velocity of 0.68 m/sec. The membrane capacity was calculated from the time constant of the foot potential and the conduction velocity to be 0.76 µF/cm2. The responses of the papillary muscle membrane to intracellular stimulation differed from those to extracellular stimulation applied with the partition method in the following ways: higher threshold potential, shorter latency for the active response, linearity of the current-voltage relationship, and no reduction in the membrane resistance at the crest of the action potential during current flow.


1984 ◽  
Vol 246 (1) ◽  
pp. H8-H16 ◽  
Author(s):  
D. Burkhoff ◽  
D. T. Yue ◽  
M. R. Franz ◽  
W. C. Hunter ◽  
K. Sagawa

We measured cardiac mechanical restitution curves, which describe the time course of recovery of ventricular contractile strength following a steady-state beat. In the first series of experiments, we studied left ventricles that beat isovolumically throughout the experiment, allowing use of dP/dtmax as a reliable index of contractile strength independent of the influence of changing ventricular pre- and afterload. The commencement of mechanical restitution was found to be associated with the onset of electrical diastole; thereafter, contractile strength rose monoexponentially to a plateau that was maintained for test pulse intervals as long as 15 s. The time constant of restitution (typically 245 ms) was independent of priming frequency and ventricular volume. These findings were interpreted in terms of a model of intracellular calcium fluxes within the myocardial cells. In a second series of experiments, we measured mechanical restitution curves from isolated ventricles that ejected against a simulated arterial impedance system. Under this condition, we did not observe the monoexponential time course of mechanical restitution as was measured under isovolumic conditions. The differences between the mechanical restitution curves measured under isovolumic and ejecting conditions were attributed to the influences of changing hemodynamic conditions on dP/dtmax that caused it to be an unreliable index of contractile strength.


1968 ◽  
Vol 11 (4) ◽  
pp. 842-852 ◽  
Author(s):  
H. N. Wright

Previous findings on the threshold for tones as a function of their duration have suggested that such functions may be systematically affected by sensori-neural hearing losses of cochlear origin. The present series of investigations was designed to explore this relation further and to determine also whether the amount of hearing loss present has any effect upon the results which are obtained. Preliminary studies were also carried out on a conductively impaired listener to indicate whether hearing losses of this type affect the threshold-duration function. The results indicate that the threshold-duration function is systematically affected by sensori-neural hearing losses of cochlear origin. This effect is manifested by a progressive shortening of the time constant relating threshold to duration and is not uniquely related to the amount of hearing loss present. The results obtained from the conductively impaired listener suggested that this type of hearing loss has no effect on the threshold-duration function, thereby implying that such functions may contribute significantly to the differential diagnosis of auditory disorders.


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