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Biomedical subjects

G Elzinga

Publications and source records attributed to G Elzinga.

At least 91 records · Page 5Linked to original sources
PubMed1982

Residual force enhancement after stretch of contracting frog single muscle fibers.

Single fibers from the tibialis anterior muscle of Rana temporaria at 0.8-3.8 degrees C were subjected to long tetani lasting up to 8 s. Stretch of the fiber early in the tetanus caused an enhancement of force above the isometric control level which decayed only slowly and stayed higher throughout the contraction. This residual enhancement was uninfluenced by velocity of stretch and occurred only on the descending limb of the length-tension curve. The absolute magnitude of the effect increased with sarcomere length to a maximum at approximately 2.9 micrometers and then declined. The phenomenon was further characterized by its dependence on the amplitude of stretch. The final force level reached after stretch was usually higher than the isometric force level corresponding to the starting length of the stretch. The possibility that the phenomenon was caused by nonuniformity of sarcomere length along the fiber was examined by (a) laser diffraction studies that showed sarcomere stretch at all locations and (b) studies of 9-10 segments of approximately 0.6-0.7 mm along the entire fiber, which all elongated during stretch. Length-clamped segments showed residual force enhancement after stretch when compared with the tetanus produced by the same segment held at the short length as well as at the long length. It is concluded that residual force enhancement after stretch is a property shown by all individual segments along the fiber.

Animals↗
PubMed1982

Electrical and mechanical responses of the intact rabbit heart in relation to the excitation interval. A comparison with the isolated papillary muscle preparation.

Experiments were performed on anesthetized open thorax rabbits with complete heart block and on isolated papillary muscles from rabbit hearts. Both preparations were basically paced at 1.0 Hz. Two consecutive test stimuli (denoted 1 and 2, respectively) were applied at various intervals. Action potentials were recorded; using suction electrodes in the intact heart and microelectrodes in the isolated tissue. Peak rate of rise of left ventricular pressure (DP) and of isometric force (DF, in vitro) were taken as measures of the contractile response. Action potential duration (AP), at 50% repolarization, were longer in vivo (175 ms) than in vitro (130 ms). AP and DP (DF) of the test contractions were similarly related to the test pulse intervals in the two preparations. DP2 was significantly correlated with DP1 and AP1 (r: 0.92-0.96). The regression coefficient for the dependence of DP2 on DP1 was significantly greater in vivo (0.61) than in vitro (0.21). This was interpreted to mean that recirculation of activator calcium from one heart beat to another was greater in vivo than in vitro. The isolated tissue would therefore be more dependent on calcium entering during the action potential. This could explain the greater postextrasystolic potentiation in vitro than in vivo (255% and 141% of steady state-responses, respectively).

Action Potentials↗
PubMed1982

Left ventricular energetics. Heat loss and temperature distribution of canine myocardium.

The sum of total left ventricular heat loss and left ventricular mean total external power was compared with the product of oxygen consumption and its energy equivalent. Myocardial blood flow, measured with 15 +/- 3 micrometers radioactive microspheres, was multiplied by the transcoronary arteriovenous temperature difference and by oxygen content difference to obtain coronary heat loss and oxygen consumption, respectively. Since only part of the heat is carried away by the coronary system a thermodilution technique was used to obtain the ratio between the heat removed by the coronary system and the external heat loss. A correction was made for the endothermic reactions of hemoglobin deoxygenation and carbon dioxide reactions with blood. Left ventricular oxygen consumption corresponded to 2.26 +/- 0.66 W/100 g, and for the sum of total left, ventricular heat loss and external power, 2.09 +/- 0.51 W/100 g was found (n = 14). In a second series, the measured transmyocardial temperature distribution was compared with the calculated temperature distribution, assuming that heat production in the myocardium is uniform and that heat is lost by coronary flow and diffusion. When thoracic and luminal myocardial surface temperatures were about equal, blood flow was found to be about the same in the various layers of the heart, whereas myocardial temperature was found to be highest near the middle of the wall (0.36 +/ 0.07 degrees C warmer than luminal temperature (n = 6). When thoracic surface temperature was increased or decreased (by + 1.56 +/- 0.99 degrees and -1.10 +/- 0.59 degrees C, respectively), consistent changes were seen for the temperature distribution in the myocardium, but not for the local flow (endo/epi ratio: 1.06 +/- 0.29 and 0.96 +/- 0.21, respectively). These data suggest that myocardial blood flow is independent of tissue temperature.

Animals↗
PubMed1982

Isolated cat trabeculae in a simulated feline heart and arterial system. Contractile basis of cardiac pump function.

Isolated cat trabeculae were studied under conditions resembling those present for the muscle fibers in the wall of the left ventricle. To obtain such a situation experimental animals, perfusion fluid, temperature, stimulation frequency, peak stress values, contraction sequence, length, and force control were chosen with respect to that criterion. Results were compared with those described for the intact feline heart in previous studies. Special emphasis was placed on determinants of the pump function graph, i.e., the relationship between mean ventricular pressure and output. It was found that peak isometric stress values measured in the trabeculae were about twice as high as those existing on average at the base of the intact left ventricle in the circumferential direction. However, the duration of the mechanical activity, as measured in iso(volu)metric contractions, was in the isolated trabeculae (206 msec) significantly less (P less than 0.01) than found in intact right (292 msec) or intact left ventricle (344 msec). Furthermore the (maximum) output of the intact left ventricle at end-diastolic pressure could not be accounted for in a simple manner by the maximum amount of shortening found in isolated trabeculae. The points of the pump function graph obtained by varying the input impedance of the loading arterial system over a wide range of compliance and resistance values in the steady state deviated only little from the graph obtained from a series of constant pressure levels applied in a beat-to-beat fashion. Therefore, the insensitivity of the pump function graph to the nature of the arterial load is found in the intact heart as well as in isolated cardiac muscle.

Animals↗
PubMed1981

Critical sarcomere extension required to recruit a decaying component of extra force during stretch in tetanic contractions of frog skeletal muscle fibers.

29 single frog skeletal muscle fibers were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a critical length change (average: 16.6 nm per one-half sarcomere) that was independent of velocity of stretch and of sarcomere length between 1.8 and 2.8 microns. After stretch there was an early decaying force component with a force-extension curve similar to that during stretch, which disappeared over approximately 2 s. This component was removed by a small, quick release, leaving a longer-lasting component. The critical amplitude of release required to produce this result was found by clamping the fiber to a load at which there was zero velocity of shortening. This amplitude increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch, and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch required to reach the breakpoint of force enhancement during stretch but was also independent of sarcomere length. The force drop accompanying the critical release showed a small increase up to an optimum magnitude at 2.4--2.7 microns sarcomere length, with a decrease at longer lengths.

Animals↗
PubMed1981

Control of cardiac output in exercising dogs using different types of workload.

The system which controls cardiac output was studied in dogs during exercise on the treadmill. The aim was to investigate whether the pattern of the workload influences the control system. To measure cardiac output, electromagnetic flow probes were implanted at least 10 days before the exercise study. During the experiments cardiac output was computed on a beat-to-beat basis. We compared changes in cardiac output resulting from stepwise, sinusoidally and randomly varying workloads, obtained by changing treadmill velocity accordingly. The time constants found with sinusoidally and randomly varying workloads were 11.6 and 10.0s respectively. The time constants of the alteration in cardiac output resulting from a step function was 9.9s for the positive step and 15.6s for the negative step. However when the stepwise change in workload was between a velocity of 0.67 and 1.56 m.s-1 positive and negative steps yielded the same time constant (13.5 s). It is concluded that the pattern of the workload has no influence on the control system of cardiac output during exercise.

Animals↗
PubMed1981

The action-potential duration and contractile response of the intact heart related to the preceding interval and the preceding beat in the dog and cat.

1. Simultaneous measurements were made in anaesthetized dogs of monophasic action potentials from the right ventricle and of the maximum rate of rise of left ventricular pressure (dP(lv)/dt(max)). Atrio-ventricular dissociation was induced and the heart paced via right ventricular electrodes.2. A control period of steady pacing was followed by a test stimulus after a variable interval called the ;test-pulse interval'. The duration of the action potential of the test beat (measured at 70% repolarization) increased with test-pulse interval and reached an approximately steady value at intervals of 1.0-1.5 sec. This constitutes the ;electrical restitution curve'.3. An increase in the frequency of stimulation prior to the introduction of the test pulses caused a downward displacement of the electrical restitution curve.4. Stimulation at 2 Hz and paired pulse stimulation at 1 Hz (same number of stimuli per min) were introduced prior to the test pulses and produced very similar electrical restitution curves.5. For a constant frequency of stimulation in the control period, adrenaline produced downward displacement of the restitution curve.6. It is concluded that there is no obvious relationship between the restitution of the action potential duration and of the contractile response. We suggest therefore that electrical and mechanical restitution occur through separate processes, the former through time-dependent recovery in membrane conductances and the latter through time-dependent increase in availability of intracellular calcium for release.7. Contractions were introduced with a test-pulse interval shorter than the optimum, and were followed by a second test pulse fixed at the optimum interval of 0.8-1.0 sec. The second test beats were potentiated (post-extrasystolic potentiation). In isolated ejecting cat hearts, there was an optimum interval for the first test pulse to produce the greatest potentiation of the second test beat. This interval was 0.2-0.3 sec, and was shortened by an increase in frequency of stimulation prior to the first test beat.8. The interval preceding the first test pulse was then varied within a range (0.8-2.0 sec) which did not produce potentiation. These first test pulses were sometimes preceded by one extrasystole. The timing of this extrasystole was altered to vary the post-extrastolic potentiation of the first test pulse.9. Multiple regression analysis, carried out between dP(lv)/dt(max) of the second test pulse (DP(2), the dependent variable) and the action potential duration (AP(1)) and dP(lv)/dt(max) (DP(1)) of the first test pulse (independent variables) yielded correlation coefficients between 0.88 and 0.99. Each determination of the coefficient included data from beats with and without post-extrasystolic potentiation.10. It is postulated that the coefficient relating DP(2) to DP(1) in the multiple regression analysis (mean value 0.75) is an index of the proportion of calcium stored during relaxation which is released again on the next beat.11. When the decay of post-extrasystolic potentiation was examined in consecutive beats at the optimum interval, the action potential durations of these beats were found to be nearly constant. A plot of dP(lv)/dt(max) of each beat against dP(lv)/dt(max) of the previous beat yielded a curvilinear relationship which was less steep than that relating DP(2) to DP(1) in the two test pulse analysis; this was attributed to inconstancy of calcium ion entry during the action potential.

Action Potentials↗
PubMed1981

"Pressure-volume" relations in isolated cat trabecula.

We studied isolated cat trabecula under conditions closely resembling those present for muscle fibers in the left ventricular wall. The purpose of the study was to see if muscle contraction under those circumstances could be described by a time-varying compliance as reported for intact canine left ventricle. We found the time of the end of systole to depend on the history of contraction. This time varied between 100 and 160 msec as measured from the onset of contraction. Similar dependency, although less percentage-wise, was found by reanalysis for intact feline left ventricles. We conclude that the behavior of the canine left ventricle as a time-varying compliance may be related to the complex organization of the cardiac muscle fibers in the wall of the heart rather than to muscle properties.

Animals↗
PubMed1980

Changes of microsphere density with time in myocardial infarcts in dogs.

The density of microspheres injected before occlusion of a coronary artery, in the infarcted region [I], was compared with that of healthy, normal myocardium [N], from the same dog. The [I]/[N] ratio was measured at different days after infarction up to 2 weeks. The ratio was below unity before the ninth day and above that thereafter. The changes in microspheres density can be explained on the basis of microsphere loss from necrotic tissue and changes in infarct mass.

Animals↗
PubMed1980

Pump function of the feline left heart: changes with heart rate and its bearing on the energy balance.

Pump function of the feline left heart was determined by measuring the relationship between mean left ventricular pressure and mean left ventricular output, obtained by changing the arterial load on a beat-to-beat basis. The effect of a change in heart rate from 120 to 160 beats . min-1 was studied and a parallel shift of the pump function graph was found. Care was taken to keep left ventricular end-diastolic pressure constant with the change in frequency. If the mean pressure and output values obtained at 160 beats . min-1 were multiplied by the ratio between the two frequencies (0.75), almost complete superposition of the two graphs was obtained. Changes in arterial load also caused changes in oxygen consumption, mean external power and external efficiency of the heart. We plotted these variables, altered them as a function of mean left ventricular output for easy comparison with the pump function graph. It was found that oxygen consumption decreases with increasing output. Mean external power and efficiency attain maxima for different values of mean output. If the left heart in the intact animal is controlled to function at its maximum power output, this can therefore not be achieved at the optimum efficiency level. The results of the present study and those obtained earlier were compared with the behaviour of a time varying compliance model.

Animals↗
PubMed1980

Measurement of left ventricular wall stress.

Forces in the myocardial wall can be measured in several ways or calculated using certain simplifying assumptions. In this study we investigated the reliability of two measurement methods, one of which was introduced by Feigl et al (1967), whereas the other method was developed in our laboratory. Both methods were tested in actively contracting skeletal muscle and beating hearts of open-chest dogs by comparing the force transferred from the muscle to the transducer under various circumstances. It appeared that changes in muscle length, be it through initial length changes or through shortening during contractions, had a great influence on the transfer of force to the transducer, for both methods, in both preparations. In the heart a decrease in internal left ventricular diameter of 15% resulted in a 50% reduction of force transferred to the transducer, independent of whether the length took place as a change in filling or as a change in ejection volume. In skeletal muscle the length-dependent effects during shortening were larger and those resulting from initial length changes were more variable than in beating hearts. That the effects of muscle length changes are of such magnitude means that, if no other errors exist, they alone would invalidate that until principally different methods of measuring wall stress in the myocardium are discovered, attempts at accurate calculation of myocardial wall stress are a better approach than wall stress measurements.

Animals↗
PubMed1980

The contractile state of cat and dog heart in relation to the interval between beats.

We induced atrioventricular dissociation and initiated ventricular pacing in intact dogs and isolated cat hearts. Left ventricular pressure, its time derivative (dP/t), and action potentials were recorded. When a test pulse was introduced at varying intervals after a period of steady pacing, an optimum contractile response was obtained at an average interval of 720 msec. A similar optimum interval was obtained after pacing at various frequencies and after paired pulse stimulation but was shortened to 560 msec after infusion of epinephrine. The magnitude of the optimum contractile response increased with an increase in the frequency of prior pacing which was accompanied by an increase in the time the cell membrane was depolarized. The optimum contractile response following paired pulse stimulation was greater than that following regular pacing, with the same number of stimuli per minute and the same time of membrane depolarization. The results are explicable in terms of intracellular calcium ion recirculation with separate compartments for release to and uptake from the contractile proteins. A negative feedback control of Ca2+ inflow to the cell by intracellular Ca2+ content is postulated to explain the effect of paired pulse stimulation and shortening of action potential duration following an increase in regular pacing frequency.

Animals↗