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Biomedical subjects

P Schiereck

Publications and source records attributed to P Schiereck.

35 records · Page 2Linked to original sources

Caffeine suppresses length dependency of Ca2+ sensitivity of skinned striated muscle.

Freeze-dried skinned cardiac and skeletal muscle preparations of the rabbit were immersed in Ca2+-containing solutions with different concentrations of caffeine. The relation between the negative logarithm of the Ca2+ concentration (pCa) and normalized developed force was studied. The exact position of these Ca2+-sensitivity functions proved to be dependent on both the sarcomere length (monitored by means of laser diffraction) and caffeine concentration. High concentrations of caffeine induce a reversible fall in tension, particularly at low binding site saturation (low pCa) and long sarcomere lengths. At a concentration of 10 mM caffeine, the sarcomere length dependency of the Ca2+-sensitivity curves is markedly reduced for the rising part of the curve. Only the depressive effect of caffeine at high pCa remains. A possible mechanism of caffeine action is discussed.

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Relaxation time constant of isolated rabbit left ventricle.

Experiments were performed on isolated rabbit left ventricles. Controlled ejections during otherwise isovolumic contractions were studied. The time constant of relaxation was defined as the slope of the linear approximation of the ln(P)-t relation over a 40-ms period starting 20 ms after the minimum of the first time derivative of left ventricular pressure (dP/dt) of the isovolumic contraction. Variations in time of ejection, its amplitude, and velocity are applied independently. No direct effect of the variations in time and velocity of the ejection on the time constant of relaxation was found. This is in conflict with the findings of Hori et al. (Circ. Res. 55: 31-38, 1984). The difference is due to the influence of the recovery of pressure directly after the end of ejection in their study. This effect is present especially when ejection was timed to take place late in the contraction phase. The effect of the variation of the amplitude of the ejection on the time constant was similar to the effect of the end-diastolic pressure on the end-diastolic volume. It is concluded that the time constant of relaxation depends linearly on the same processes that are responsible for the height of the end-diastolic pressure.

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High-speed transient-recording microprocessor system for the analysis of asymmetrical diffraction spectra from striated muscle.

A microprocessor based digital recording system has been developed to study the fine structure and asymmetry of diffraction spectra from striated muscle during contraction. Two linear 256-element photodiode arrays provide analog videosignals of the diffraction lines imaged onto these charged coupled devices. The photodiode arrays are alternately read and the videosignals can be digitized and stored within 1.36 ms (two images of 256 points) with a spatial resolution of 5 nm. (In this paper the spatial resolution is considered to be the standard deviation of the first-order maximum of a monochromatic wave of the He/Ne laser measured from the diode-arrays, using ideal gratings with a spacing between 1.6 and 3.6 microns.) The system's memory with a capacity of 192 pairs of images of 256 points can be optimized by means of a threshold to contain about 2000 images without any loss of information. A transient recording approach makes the system capable of recording long term slow phenomena of up to 5 s as well as fast events and the combination of fast events within slow processes. The system presented here has a significantly improved time resolution and storage capacity when compared to other systems and is more versatile. This is the first system which enables the simultaneous examination of the fine structure and asymmetry of diffraction spectra.

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Immediate effects of diastolic loading variations on the left ventricular inotropic state in open chest dogs.

The influence of left ventricular filling and variations in end diastolic volume on cardiac performance was studied in the intact dog heart. Left ventricular filling volumes and stroke volumes were calculated on a beat to beat basis from measurements of natural mitral inflow and aortic outflow obtained by electromagnetic flow sensors. Instantaneous controlled modifications of end diastolic volume were performed through a cannula situated in the left ventricle and connected to a pump system outside the dog. This system enabled controlled increases or decreases of the end diastolic volume at any prechosen moment during the diastolic pause. Absolute volume variations in end diastolic volume and end systolic volumes could be calculated by combining the integrated flow signals from different consecutive beats. Left ventricular performance was evaluated in terms of end systolic volume and end systolic pressure variations. When the diastolic volume was abruptly increased by the pump system, natural mitral inflow decreased but end diastolic volume increased. The effect on diastolic pressure was dependent on the variation in filling rate, the amplitude of the infusion, the moment at which the infusion was started, and the diastolic pressure at the start of the infusion. Also stroke volume, maximal systolic pressure (Pmax), end systolic pressure, and end diastolic volume increased. The increased systolic performance was attributed to the increased end diastolic volume as expected according to Starling's law. When end diastolic volume was rapidly decreased during diastole by the pump, natural filling volumes increased to compensate for the volume loss by the pump. End diastolic volume was, however, smaller indicating that full compensation was not achieved. Evaluation of ventricular performance in terms of end systolic pressure and end systolic volume showed a decreased end systolic pressure and increased end systolic volume compared with the control values. The effect of a pump withdrawal was 1.62(0.38) times larger than could be explained on the basis of Starling's law. After the infusion of adrenaline the intrinsic depression disappeared and the influence of the volume withdrawal on cardiac performance was as expected from the Starling mechanism.

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End-systolic pressure-volume relations of isolated ejecting rabbit left ventricles after quick diastolic volume changes.

The aim of the study was to investigate the influence of quick diastolic volume changes on systolic performance of ejecting left ventricles. To measure left ventricular systolic performance the maximum ratio of ventricular pressure (P) and volume (V) was calculated on beat-to-beat basis when the diastolic loading conditions were varied in different ways. These end-systolic P-V (P-VES) points were obtained from both isovolumic and ejecting contractions. A deviation from the P-VES relation is thought to result from factors changing the inotropic condition of the heart. When steady state isovolumic and ejecting P-VES data were collected linear P-VES relations were found. The relations coincided when stroke volumes were not too large. When the diastolic volume was quickly changed (ie 10 to 20 ms) late in diastole, the P-VES points of the resulting contractions showed a significant deviation from the steady state relation (p less than 0.001). This deviation was dependent on the magnitude of the volume step. After quick volume infusions the heart ejected to end-systolic volume (ESV) values that were smaller than expected from the steady state P-VES relation and the end-systolic pressure (ESP) was larger. After quick volume withdrawals ESV values were larger and ESP was smaller than expected. The magnitude of the effect was not dependent on the preset basic diastolic volume if the volume changes were considered as fractions end-diastolic volumes (EDV). It is concluded that when diastolic volumes are varied just before stimulation, a significant deviation of the P-VES point from the steady state P-VES relation is found in the following contraction. This phenomenon suggests an alteration in the inotropic state of the heart.

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Influence of the velocity of changes in end-diastolic volume on the starling mechanism of isolated left ventricles.

1. In this study the relationships between active developed systolic pressure, end-diastolic pressure and different diastolic volumes are studied in Tyrode perfused isolated rabbit left ventricles. Contractions were isovolumic. 2. Rapid diastolic volume changes were imposed on top of different preset basic diastolic volumes. These volume changes are shown to produce systolic and diastolic pressure values that cannot be explained by assuming a single pressure-volume relation during systole and diastole. The changes in pressure are in the same direction but higher than is expected on the basis of the increase or decrease of the ventricular end-diastolic volume alone. 3. The variation of the diastolic pressure-volume relation cannot be explained by assuming variations of the heart's passive elasticity or viscous effects within its wall. During diastole the effect is completely reversible without concomitant systolic effects. No velocity dependent effect of the quick volume change could be observed if the time duration was varied between 10 and 65 ms. The results are in keeping with the hypothesis that active force generating mechanisms may be present during the diastolic pause. 4. The effects observed during systole suggest the possibility of length dependent activation of the myocardial cells. This results in different inotropic conditions of the heart at identical volumes, depending on how these volumes were installed. These volumes may be considered to affect intrinsic properties of the muscle cells on a beat to beat basis.

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The effect of some sex hormones on the isovolumetric pressure curve of the rabbit's left ventricle.

The effect of some sex hormones (estradiol-17 alpha), estradiol-17 beta, estrone, progesterone and testosterone) on the mechanical activity of rabbit left ventricle was studied in concentrations within the physiological range. Investigations were carried out during the first ten minutes after the introduction of the steroid. Only progesterone and estradiol-17 beta affect the isovolumetric pressure curve; the other steroids do not exhibit any effect. The effects of estradiol-17 beta and progesterone counterbalance each other. Estradiol-17 beta enhances the rate of pressure development and decreases the time to reach peak pressure. Progesterone decreases both the rate of pressure development and the time to reach peak pressure.

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Non-linear pressure development during velocity controlled volume releases in isolated contracting rabbit left ventricle.

Pressure responses obtained during steady-volume releases performed on isolated contracting rabbit left ventricle reveal a typical non-linear time course, dependent on velocity of volume release (VVR) and on amplitude of volume release (AVR). For values of VVR = 4.8 ml/s and of AVR = 0.28 ml (about 20% of the EDV at preload 0.5 kPa) a shoulder shaped pressure-time course is observed. The shoulder is seen during releases independently of the time during systole at which the release starts. When releases are compared which start at the same time during systole but have different velocities then the shoulder appears at higher amplitudes for the higher velocities. The shoulder can be explained by an active actin-myosin interaction within the scheme of a multi-state contraction model.

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Left ventricular active stiffness: dependency on time and inotropic state.

Left ventricular systolic stiffness was measured by rapidly changing ventricular volume (within 7 ms) of isovolumically contracting isolated rabbit hearts. Instantaneous pressure-volume relations were found to be linear with slopes that depended upon the moment during contraction at which the volume change was induced. These slopes were proportional to the total pressure developed in the ventricle just prior to the volume change. The same was found when the time course of pressure was influenced by changing the Ca++ content of the perfusate. An influence, however, also could be detected when end-diastolic volume was changed. At the same pre-release pressure a greater volume caused a decrease of active stiffness. The results indicate the possibility of an active component in ventricular systolic stiffness.

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The effect of controlled changes in volume on the active state of the rabbit isolated left ventricle.

The contractile properties of isovolumically contracting isolated rabbit left ventricles are studied under the influence of controlled rapid volume changes during systole and diastole. The time integral of the pressure curve (TTI), representing the active state, is used to quantify the energy consumption of the ventricle. Steady state conditions resulting from an introduced volume change show a TTI/EDV relation which represents the Starling curve. However, immediately after a quick volume increase (decrease) introduced in diastole, the TTI/EDV ratio has a higher (lower) value than indicated by the Starling relation. This shows a volume dependent activation (deactivation), related to changes in the inotropic state of the heart muscle cells within the ventricular wall. A volume increase at a later moment (in systole) always produces a lower rate of activation. Indeed, if the rapid volume change is introduced at moments later than 70% of time to peak pressure, TTI is less than observed from the Starling mechanism, indicating a deactivation. When comparing the decreasing effect on the active state introduced by volume decrease during systole, it is shown that this effect is not only a function of the amplitude of the decrease itself but is highly dependent upon the way EDV is reached.

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Effect of sarcomere length and filament lattice spacing on force development in skinned cardiac and skeletal muscle preparations from the rabbit.

Skinned cardiac and skeletal muscle freeze-dried preparations were activated in solutions strongly buffered for Ca2+. The response of single skeletal muscle fibres or thin strips of papillary muscle was investigated in relation to changes in Ca content of the perfusate. Sarcomere length was set and controlled during the experiments. The relation between the negative logarithm of the Ca concentration, the pCa, and the normalized developed force proved to be sigmoidal. The exact position of these curves proved to be dependent upon both sarcomere length and the distance between the filaments. The latter was shown by means of osmotic compression of the fibres using dextran. As a consequence of these observations, it was concluded that the length-tension relation is dependent upon the actual Ca concentration. The results are discussed in terms of cross-bridge interaction.

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