The relation between left-ventricular stroke volume (SV) and end-diastolic volume (EDV) was determined based on angiocardiographic measurements in 10 open-chest minipigs under varying filling conditions (blood letting or infusions). The results were compared with a theoretical relation calculated under the assumption of varying EDV but constancy of myocardial properties. In contrast to the linear increase of SV as a function of EDV as found in the animal experiments, the calculated curve reveals a maximum near the normal operating point with a decrease in the range of higher EDV. It can be concluded that the well-known increase of SV with increasing ventricular filling, beyond the normal EDV, is almost completely due to muscle physiological factors (mainly increase in Ca2+ sensitivity of the contractile apparatus), whereas the decrease of SV in the range of low filling pressure is mainly due to the geometrical conditions.

Angiocardiography↗

PubMedDate not supplied

[Alterations in the passive and active performance of cat papillary muscle induced by variation of preload (author's transl)].

In the isolated cat papillary muscle a rapid change in length induces a viscoelastic process of relaxation, during which the diastolic tension attains its new equilibrium after a delay. Its time course may be approximated both after stretching and releasing by a total of four exponential functions being marked by highly diverse time constants. During the stretch-induced relaxation phase the isometrically active papillary muscle shows a marked increase in mechanogram amplitudes, which is preceded in the first seconds by a short-term decrease. An opposite behavior is to be recorded after abrupt releases. The mechanograms of the stationary state prove to be exclusively a function of the degree of stretch, while the contractions in the early relaxation phases are dependent on the speed, direction and scale of the preceding change in length. The higher the stretching step chosen, the more clearly reduced are the mechanogram amplitudes of the early relaxation phase in comparison to the stationary state. This applies especially right of the optimum of force-development and contradicts a viscoelastic interpretation of the systolic phenomena in the poststretch phase. The findings after abrupt stretching point to either an initial decrease of amplitude or to a delayed approach of the contractions to their stationary state. Stretch-induced changes in the time course of the action potentials would constitute an adequate basis for the interpretation of these phenomena.

Animals↗

PubMedDate not supplied

Myocardial function in different models of cardiac hypertrophy. An attempt at correlating mechanical, biochemical, and morphological parameters.

Based on mechanical, biochemical and electron microscopic studies performed in the same stage of experimental cardiac hypertrophy, an attempt is made to define the significance of individual factors responsible for the alterations in myocardial function. Using swimming rats, it is demonstrated that a load-induced increase in cardiac mass is not necessarily connected with an impairment of contractile capability on a cellular level. Yet, also, the reduction of specific ATPase activity and unloaded shortening velocity in pressure-induced hypertrophy (goldblatt rats; aortic stenosis) seems to be the expression of adaptation rather than of cellular damage, at least in the earlier stages. Although there are distinct indications of alterations in Ca-dependent activation and deactivation, in the Goldblatt model electromechanical coupling does not seem to be the main cause of altered contraction parameters. The correlation between specific ATPase activity of actomyosin and unloaded shortening velocity as well as the persistance of decrease in shortening velocity, also under optimal electromechanical coupling conditions, point to an inner relationship between the two values. A discrepancy between unloaded shortening velocity on the one hand and developed tension on the other is mainly due to an increased content of contractile structures. In later stages, an increased connective tissue content influences both isometric and isotonic parameters.

Actomyosin↗

PubMedDate not supplied

Time course of electron microscopic alterations in the hypertrophied myocardium of Goldblatt rats.

In Goldblatt rats, electron microscopic investigations of morphological changes in heart tissue during the compensatroy stage of pressure induced cardiac hypertrophy were performed. Myocardial cellular size enlarged considerably within the first 4 weeks after renal artery coarctation. An enlargement of the T-tubular system is particularly striking. The ratio of myofibril volume to total cell volume is significantly increased from the 4th-24th week and can at least partially explain a rise in developed tension which occurs in spite of a frequent disarrangement of myofibrils. In later stages severe changes in the vessel walls take place and there is an augmentation of connective tissue which impairs a correlation between myocardial cell alterations and mechanical parameters.

Animals↗

PubMedDate not supplied

Mechanics of the isolated ventricular myocardium of rats conditioned by physical training.

Force-velocity relations from after-loaded contractions, from isometric and isotonic QR experiments, resting-tension curves and biochemical analyses were conducted on sixteen trabecular muscles (SH) from hearts of rats conditioned by eight weeks of swimming training (increase in heart weight 8%), and compared to a control (CH) of eighteen trabecular muscles. (SH) showed increased tension development (p less than 0.01), whereas the diastolic properties remained almost unchanged. Analysis of the amount of hydroxyproline did not prove any variation. Vmax of (SH) was only slightly increase when there was a singificnat rise in actomyosin and myosin ATPase activity, while PO of the force-velocity relations of (SH) on the x axis (tension) shifted clearly to the right (p less than 0.01). Consequently, the maximum instantaneous power of (SH), expressed by the maximum rectangular plane under the force-velocity curve, increased considerably (p less than 0.01) in comparison with (CH). The experiments show that haemodynamic load induced by training does not alter the passive properties of the myocardium, but does bring about an increase in the contractile capabiltiy.

Actomyosin↗

PubMedDate not supplied

[Evaluation of elasticity by means of length-tension relationships in a model of isolated ventricular myocardium from rat and cat papillary muscle under conditions of contracture (author's transl)].

Increase of Ca2+ concentration to 7.5 mM in the presence of 10 mM or 20 mM caffeine shifted length-tension relationships of 5 rat trabecular muscles and 5 cat papillary muscles to higher tensions. At 1max diastolic tension was enhanced from (formula: see text), for all measured points of stress-strain relationships after the increase of diastolic tension by caffeine and Ca2+ as well as under control conditions. The function E = f (sigma) = b (sigma - c) was computed by linear regression analysis (0.99 greater than r2 greater than 0.96). The average value of constant b was 13.89 +/- 2.01 in control curves of rat trabecular muscles and 13.42 +/- 1.98 in curves with 10 mM caffeine and 7.5 mM Ca2+. Likewise, in cat papillary muscles 20 mM caffeine and 7.5 mM Ca2+ did not alter the stiffness constant b in a statistically significant manner (control: 16.63 +/- 3.03, caffeine: 16.43 +/- 3.02). The results demonstrate that the stiffness constant b cannot indicate acute variations of the length-tension relationships due to caffeine and Ca2+ and may result in overestimating of myocardial distensibility. However, if the tangent modulus (E) is related to strain (epsilon), the alterations of diastolic elasticity are detectable. Mathematical considerations of these experimental results imply a new base for evaluation of diastolic elasticity of the heart by means of the tangent modulus (E). These results are of substantial importance in clinical evaluation of distensibility of myocardial tissue, as the tangent modulus related to wall stress apparently is not appropriate to realize alterations in "passive" myocardial properties due to contracture.

Animals↗

PubMedDate not supplied

Connective tissue content and myocardial stiffness in pressure overload hypertrophy. A combined study of morphologic, morphometric, biochemical, and mechanical parameters.

We investigated samples of left ventricular myocardium from Goldblatt II (4 and 8 weeks after operation) and spontaneously hypertensive rats (SHR; 40 and 80 weeks old) by histological and morphometric methods. From the same hearts, the distensibility of the left ventricular papillary muscle was analyzed by means of resting tension curves, and the collagen content of the whole left ventricular wall was determined by means of hydroxyproline concentration. In all groups, myocardial fibrosis was observed to accompany myocardial hypertrophy. The severity of fibrotic lesions increased with the duration of hypertension, and, in late stages, degenerative changes of cardiac myocytes were found. Morphometric determinations and chemical analysis of the hydroxyproline concentration revealed a decrease in myocardial muscle content, which was paralleled by an increase in collagen content when compared to the respective controls. In general, morphometric and chemical findings correlate with increased myocardial stiffness observed during mechanical measurements in isolated papillary muscle preparations from the same hearts. Differences were found, however, between chemical analysis and mechanical measurements in the 40-week-old SHR group, which may result from different patterns of collagen distribution between interstitium, perivascular spaces, and the walls of blood vessels. The comparison between histological, morphometric, chemical, and physiological data shows that (1) cardiac hypertrophy of Goldblatt and SH-rats is accompanied by myocardial fibrosis, and (2) changes in passive elastic properties of myocardium is better reflected in morphometric than in chemical analysis.

Animals↗

PubMedDate not supplied

Functional significance of ventricular dilatation. Reconsideration of Linzbach's concept of chronic heart failure.

On the basis of theoretical considerations and experimental data this study deals with the functional consequences of structural dilatation, particularly in view of Linzbach's concept of chronic heart failure (34-38). After a short review of the literature, a theoretical analysis of the relationship between stroke volume and ventricular inner radius is presented assuming a thick-walled sphere. Presupposing constant contractility, end-diastolic sarcomere length, end-diastolic wall thickness and end-systolic pressure, only a considerable increase of ventricular radius could be the direct cause of ventricular pumping failure - despite increasing wall stress and reduced ejection fraction. Impaired contractility, as well as insufficient hypertrophy and increased systemic pressure, would intensify the adverse consequences of ventricular enlargement to a predictable extent. Thus, hemodynamic and energetic consequences of dilation, although mutually interacting, should in principle be distinguished. Despite considerable simplifications involved in model calculations, the relative significance of contractility, ventricular size, wall thickness, and extracardiac factors (mechanical overload; neuroendocrine reactions) can be estimated in various animal models with congestive failure. Hence, this theoretical and experimental approach permits the modification and deepening of previous concepts of structural dilatation and also has implications for interpreting the effects of therapeutical interventions.

Animals↗

PubMedDate not supplied

Geometric and muscle physiological determinants of cardiac stroke volume as evaluated on the basis of model calculations.

Based on model calculations a mathematical approach has been developed which permits an analysis and approximative evaluation of the significance of geometric and various muscle physiological factors for cardiac stroke volume with respect to anatomical ventricular size. Despite increasing wall stress the stroke volume generally increases with growing anatomical heart size, reaching a maximum beyond which it falls off. On the basis of the model of a thick-walled sphere for the left ventricle, stroke-volume-radius relations have been calculated for three different types of chronic ventricular enlargement (constancy of wall thickness, wall volume, or of the ratio of wall thickness to inner radius) in particular. In all three cases stroke volume increases with chronic enlargement of the heart, at least to a certain extent. Thus, stroke volume can be augmented with increasing anatomical heart size under constant contractile conditions despite decreasing ejection fraction. This fact has to be considered in the assessment of ventricular function. Nomograms are obtained by varying contractility, wall thickness, or end-systolic pressure while keeping the other contractile conditions constant, thus permitting the evaluation of the effect of therapeutic measures in the presence of cardiac dilatation.

Heart↗

PubMedDate not supplied

The influence of endurance training on mechanical catecholamine responsiveness, beta-adrenoceptor density and myosin isoenzyme pattern of rat ventricular myocardium.

An investigation was carried out on the effects of 4 weeks' swimming training (2 X 90 min/day) on myocardial isometric tension development and rate of tension rise, and also on the changes induced therein by in vitro application of isoproterenol. This was done in 9 isolated papillary muscles of 9-week-old male Wistar rats and the results were compared with the data of age-matched sedentary controls. Ventricular beta-adrenoceptors [( 3H]-dihydroalprenolol binding) and the isoenzyme pattern of myosin (pyrophosphate gel electrophoresis) were examined in the same individuals. Isometric tension (T) and its first derivative (dT/dt) measured at the optimum of the length-tension diagram were moderately increased by long-term swimming training. Isoproterenol (10(-5) mol/l) induced a greater absolute and relative increase of both mechanical parameters in specimens of trained animals than in age-matched controls (delta T: 3.6 +/- 1.6 vs. 1.9 +/- 0.6 X 10(-2) N/mm2, p less than 0.05. delta dT/dt: 43.4 +/- 14.0 vs. 30.4 +/- 9.5 X 10(-2) N/mm2 X s, p less than 0.05). KD decreased significantly (4.23 +/- 1.0 vs. 2.44 +/- 0.3 nM, p less than 0.02), indicating an increase in receptor affinity, whereas receptor density revealed a tendency to decrease (98.8 +/- 22.6 vs. 67.1 +/- 18.0 fmol/mg protein, p less than 0.1). In addition, there was a shift in the isoenzyme pattern of myosin towards VM-1 after swimming training. Thus, under the conditions of the present experiments, the mechanical response to isoproterenol does not correlate to beta-adrenoceptor density. It is probable that, apart from the altered sensitivity of the receptors, other membrane or post-membrane processes, are responsible for the increased mechanical responsiveness to catecholamines. Although a relationship between myosin isoenzyme pattern and mechanical responsiveness to catecholamines is apparent taking into account our results and the findings on hypertensive rats as reported in the literature, it cannot be accounted for simply by altered beta-adrenoceptor density.

Adenosine Triphosphatases↗

PubMedDate not supplied

Left ventricular isovolumetric pressure-volume relations, "diastolic tone", and contractility in the rat heart after physical training.

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Animals↗

PubMedDate not supplied

Significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship under acute hypoxia in the dog.

In 14 closed-chest dogs, the significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship was investigated under acute hypoxia by means of single plane cineventriculography and simultaneous intraventricular pressure recording. Both after 5 min asphyxia (respirator switched off) (n = 5) and after 3 min hypoxia (ventilation with pure N2) (n = 9), there was a significant leftward shift (p less than 0.005) of the left ventricular enddiastolic pressure-volume curve as compared to the control curves under normoxia. To simulate the elevated filling of the right ventricle under acute hypoxia, rapid intraventricular infusion was applied under normoxic conditions to raise right ventricular enddiastolic pressure to the same values as that measured under hypoxia. The extent of the ensuing leftward shift of the left ventricular enddiastolic pressure-volume curve was on average 60% of the shift under hypoxia in both sets of experiments. Neither the slope of the relationship between volume stiffness and enddiastolic pressure, nor the relationship between tangent elastic modulus and left ventricular wall stress, was affected by hypoxia or asphyxia. Thus, the shift of the left ventricular enddiastolic pressure-volume curve in the early stage of hypoxia is predominantly due to the influence of increased right ventricular filling. Since the increased volume of the atria under acute hypoxia limits left ventricular distensibility additionally, the changes in left ventricular enddiastolic pressure-volume relationships observed in the early stage of hypoxia are mainly, or even entirely, the result of interaction of the various heart compartments, and not a reflection of alterations in myocardial tissue elasticity.

Animals↗