Maximal twitch tension in intact length-clamped ferret papillary muscles evoked by modified postextrasystolic potentiation.

Abstract

A modified test of postextrasystolic potentiation achieved with a brief episode of rapid pacing followed by a 6-second pause (RPP maneuver) was used to evoke maximal force in isolated intact ferret right ventricular papillary muscles. Maximal RPP tensions were examined under length-clamped conditions and compared with the steady-state forces obtained when further increases in [Ca2+]o, did not further increase force and to the tensions recorded at the point of saturation of force when similarly length-clamped muscles were subjected to caffeine-induced tetanization. The results show that the calculated maximal twitch tension achieved with RPP is comparable to the 25-35 g/mm2 observed in intact single skeletal muscle fibers. The study also shows that the beat-to-beat decay of the potentiated contraction is exponential. While the amount of the constant fractional beat-to-beat decay is a function of [Ca2+]o, it is not influenced by length. During the decay of potentiation, the ratio of the potentiation of any beat divided by that of the previous beat is a constant, called (X). With certain assumptions, it is shown that (X) is a measure of the fraction of activator calcium taken up by the sarcoplasmic reticulum in each beat and, in the steady state, the fraction of activator calcium that comes from the sarcoplasmic reticulum. The (X) amounted to 33%, 50%, and 65% when [Ca2+]o was 1.25, 2.50, and 5.0 mM, respectively. Thus, at 1.25 mM [Ca2+]o, some two thirds of the total calcium required to activate the myofilaments comes from the extracellular compartment during excitation and only one third is contributed via release from the sarcoplasmic reticulum. In the region of optimal myofilament overlap, RPP force-length curves are remarkably shallow and almost indistinguishable from the sarcomere length-tension relation observed in skinned single cardiac cells. Tetanus plateau tensions are significantly smaller than RPP forces at any length, and the slope of the tetanus force-length curves is greater than that obtained with RPP. Thus, and by exclusion, we also suggest that caffeine may exert significant downstream inhibitory effects.

Comparison of the effects of sevoflurane, isoflurane and halothane on rat myocardium

“…Two hypotheses can be raised: first, sevoflurane increases the amount of calcium slowly accumulated in the SR during the rest period, and second, it increases calcium release from the SR. Halothane, isoflurane and sevoflurane did not affect post-rest recovery, assessed by the rate constant, τ, of the exponential decay of AF (table 2). This suggests that halogenated anaesthetics do not significantly alter the recirculation fraction of calcium within the SR. 22 R2 tested the lusitropic state under high load and thus could indirectly reflect myofilament calcium sensitivity. Our results showed that sevoflurane and isoflurane did not significantly modify R2 ( fig.…”

“…12 τ is the number of beats required for post-rest contraction to decay to one-tenth of its maximum (B1); it is assumed to represent the time required for the SR to reset itself, and was therefore used to test SR function. 22 At the end of the study, muscle cross-sectional area was calculated from the length and weight of papillary muscle, assuming a density of 1. Shortening and lengthening velocities were expressed in lmax s 91 , force in mN mm 92 and force derivative in mN mm 92 s 91 .…”

Improved Mechanoenergetics and Cardiac Rest and Reserve Function of In Vivo Failing Heart by Calcium Sensitizer EMD-57033

“…13,14 In contrast, pure Ca 2ϩ sensitization has minimal influence on the RF. 15 All of the preceding protocols were performed in every CON animal and 7 HF dogs.…”

In-plane myocardial wall stress is not the primary determinant of coronary systolic flow impediment. A study in the isolated, perfused dog septum.

“…During each increment of stretch the effect of a reproducible, rapidly reversible increase in contractility was obtained by examining the potentiated beat of a special pacing protocol consisting of a sequence of five control beats at a frequency of 0.4 Hz and 10 beats at 10 Hz, followed after a 6-second pause by the potentiated beat. 19 The purpose of the 10 fast beats and pause is to alter the calcium cycling of the tissue so the next beat is nearly maximally potentiated, as had been verified in isolated cardiac muscle.19 These fast beats were not analyzed; rather, analysis of only the next to last control beat and the single potentiated beat provided control and nearly maximal contractility states for comparison at each step of stretching. To assess the reproducibility of the pacing sequence, we repeated the sequence five times in the unloaded state in two specimens.…”