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Biomedical subjects

G Kissling

Publications and source records attributed to G Kissling.

16 recordsLinked to original sources
PubMed1992

Mechanical determinants of myocardial oxygen consumption with special reference to external work and efficiency.

OBJECTIVE: The aim of the study was to investigate the ambiguous effect of left ventricular afterload on myocardial work, oxygen consumption, and efficiency. METHODS: Myocardial oxygen consumption and mechanical parameters of the left and right ventricle were measured in situ in a modified heart-lung preparation in the rat. Left ventricular afterload was adjusted arbitrarily by means of a Starling resistor mounted in a shunt circuit between the left ventricle and the caudal caval vein. Left and right ventricular pressure and aortic pressure as well as pulmonary flow and the flow in the shunt circuit were measured. The left ventricular pressure and volume values were converted into wall stress and length data assuming a thick walled sphere, and external work was calculated from left ventricular force and shortening. RESULTS: Left ventricular external work ran through a maximum with decreasing aortic pressure. Left ventricular oxygen consumption per gram and beat correlated linearly with left ventricular peak wall stress, tension-time integral, and maximum rate of stress development. Left ventricular force and shortening, the two components of external work, acted differently: force determined left ventricular oxygen consumption, whereas shortening had no direct effect on myocardial oxygen consumption, but was important in determining left ventricular efficiency. CONCLUSIONS: The interplay between left ventricular afterload and coronary perfusion pressure is of special significance for the heart in situ. The decrease in shortening and external work as well as the diminution in efficiency, observed at low aortic pressure values, can be attributed to impaired coronary perfusion. The coronary perfusion pressure must therefore be taken into consideration for the critical examination of the efficiency of the heart in situ.

Animals↗
PubMed1992

Functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions.

The functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions is discussed, based mainly on animal experiment results (in the dog, pig and rat). The dependence of individual stroke volume on end-diastolic volume can be described adequately using Frank's diagram. This can be illustrated by varying filling pressure (respiratory cycle, vascular tone in the capacitance system, body position, circulating blood volume) and by alterations in the duration of the filling period (heart rate and rhythm, rate of relaxation) and in ventricular compliance (wall thickness, fibrosis; contracture, rigor). The functional importance of the Frank-Starling mechanism lies mainly in adapting left to right ventricular output. During upright physical exercise an increase in end-diastolic volume due to the action of the peripheral muscle pump and increased venous tone can assist in enhancing stroke volume. Reduced contractility leads to a shift of the operating point to the right in the pressure-volume diagram, thus tending to prevent a decrease in stroke volume. However, the consequences of increased circulating blood volume in chronic heart failure are, as a rule, mainly detrimental (congestive symptoms; myocardial component of coronary resistance; cardiac energetics). Reduced contractility results in a flattening of the relation between stroke volume (or stroke work) and end-diastolic volume. Furthermore, the Starling mechanism is prevented from becoming effective if the sarcomere-length reserve is exhausted, or in the presence of inadequate sarcomere extension due to impaired relaxation or reduced distensibility of the ventricular wall. The latter is illustrated using the example of a dilated fibrotic left ventricle from a rat with experimental supravalvular aortic stenosis.

Animals↗
PubMed1991

The effect of decreased left-ventricular afterload on cardiac performance in the normal and hypertrophied rat heart.

The effect of left-ventricular afterload on cardiac performance was investigated in normotensive Wistar rats and in spontaneously hypertensive rats (10 months old) with a left-ventricular hypertrophy of 54%. The measurements were performed on a modified heart-lung preparation in which left-ventricular afterload could be adjusted arbitrarily. In the heart in situ, left-ventricular afterload limits not only the mechanical conditions of the contraction, but also influences coronary perfusion pressure. With decreasing afterload stroke volume and pressure-volume work initially increases. Simultaneously coronary resistance decreases considerably so that coronary flow increases, although coronary perfusion pressure is reduced. However, when perfusion pressure falls short of a critical value, coronary flow cannot be maintained despite maximal coronary dilatation and stroke volume decreases, i.e., stroke volume, pressure-volume work and coronary flow run through an optimum with decreasing afterload. A reduction in coronary perfusion pressure below a certain value yields acute heart failure in all preparations. The minimal aortic mean pressure without reaching cardiac insufficiency was in the spontaneously hypertensive rats with 65 mm Hg significantly higher than in the control animals with 35 mm Hg, although the minimal coronary resistance was identical in both groups. The elevated critical coronary perfusion pressure of the spontaneously hypertensive rats can be explained by the increased O2-demand of the hypertrophied hearts.

Animals↗
PubMed1990

[Validation of a Doppler catheter for intravascular flow measurement in vivo. A comparison with simultaneous electromagnetic flow measurement].

A new 3-French Doppler catheter has recently been developed for direct measurement of blood flow velocity within the vessel. In in-vitro studies Doppler and real flow measurements correlated strongly. To validate this method in-vivo, phasic flow measurements in the aorta ascendens of 11 narcotized Wistar rats using Doppler and an external electromagnetic flowmeters were performed. The individual stroke volume was varied over a wide range. High intraindividual correlations were found (r = 0.92-0.99). However, a considerable variation of the slope a of the regression lines was noted (a = 0.42-1.47). Thus, qualitative registration of phasic flow is possible and relative changes of flow can be determined with sufficient accuracy through intravascular Doppler measurements. Probably due to interindividual differences of the catheter position within the vessel, however, measurements of absolute flow volumes are unreliable in this setting.

Animals↗
PubMed1987

Chronic cardiac reactions. II. Mechanical and energetic consequences of myocardial transformation versus ventricular dilatation in the chronically pressure-loaded heart.

Mechanical and energetic consequences of myocardial transformation and of ventricular configuration on the other were separately analysed. The considerations were realized on representative samples of normotensive rats and spontaneously hypertensive rats (SHR) in compensated stages, as well as in SHR in a state of congestive cardiac failure. Cardiac dynamic measurements were performed under Urethane anaesthesia and open chest conditions. Myosin isoenzyme pattern was determined by pyrophosphate gel electrophoresis. Energetic calculations were based on oxygen consumption data, measured in a specified heart-lung model. In the compensated stage of SHR the concentric type of left ventricular hypertrophy with renormalized systolic auxotonic wall stress predominated. The process of cardiac hypertrophy was associated with a shift in the myosin isoenzyme pattern towards the "slow" VM-3. Myocardial transformation did not significantly reduce myocardial performance and pumping ability, but caused a decrease in oxygen consumption as related to developed stress and LV weight. Thus, the efficiency of the hypertrophied ventricle of SHR was improved. However, due to the moderate effect of isoenzyme pattern redistribution for total energy turnover and the limited adaptive reserve of normotensive controls, the extent of improvement was small. In SHR with congestive heart failure, myocardial contractility was severely impaired, when structural dilatation of the left ventricle had set in. Reduced myocardial contractility could not be explained solely on the basis of a shift in the myosin isoenzyme pattern. Both impaired myocardial contractility and structural dilatation contributed to reduced ventricular performance. Myocardial transformation, along with its energy economizing effect, failed to compensate for unfavorable energetic consequences of structural dilatation and therefore the reduced ventricular efficiency is assumed to be another deleterious factor in the dilated failing heart.

Animals↗
PubMed1987

Implications of myocardial transformation for cardiac energetics.

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.

Adenosine Triphosphatases↗
PubMed1987

Functional significance of contractile proteins in cardiac hypertrophy and failure.

The functional significance of alterations in contractile proteins was investigated in the chronically overloaded left ventricle of Goldblatt rats and spontaneously hypertensive rats (SHRs). Congestive cardiac insufficiency occurring in late stages of pressure overload is associated with impaired contractility, as well as significant structural dilatation. Only in the event of extreme dilatation, however, would pumping failure occur in the presence of intact myocardial contractile capability. The transformation toward a slower myocardium is associated with a reduced rate of Ca2+ uptake by the sarcoplasmic reticulum. Transformation influences ventricular and myocardial working capacity to a much lesser extent than do the velocity parameters of contraction. Although a fairly homogeneous VM-3 pattern is typical for ventricles when cardiac failure is experimentally induced, extreme myocardial transformation, as such, does not cause congestive failure. With cardiac insufficiency, left ventricular volume, systolic wall stress, and hydroxyproline concentration are overproportionately increased, as related to VM-3 content, whereas noradrenaline content is decreased. This is consistent with the assumption that myocardial transformation is not necessary for the development of these alterations. Myocardial transformation may be promoted by structural dilatation. Extreme transformation, however, should, in turn, decrease contractility, contributing to cardiac failure. A considerable decrease in contractility indirectly causes depletion of the catecholamine stores. The energy-saving effect of myocardial transformation toward a slower muscle cannot compensate for the unfavorable effects of a substantial degree of ventricular dilatation.

Animals↗
PubMed1975

Cardiac hypertrophy due to physical exercise--an example of hypertrophy without decrease of contractility: unreliability of conventional estimation of contractility by simple parameters.

In 100 young, male Sprague-Dawley rats, a long term swimming training (2 hr/day for 8-12 weeks) produced an increase in heart weight of 10 percent, and an increase of about 15 percent in the relation of heart weight to body weight compared with control rats of the same age and initial weight. In examinations of the mechanical properties of the whole ventricle as well as of trabecular preparations, there was no evidence of impaired myocardial contractile ability because of the swimming training. Some parameters for the estimation of "contractility" increased, whereas others decreased. At a muscle length near lmax, the developed force and the maximal rate of force development were slightly augmented. The results reveal the limited value of some indices of contractility. Alterations in the shape of the contraction curve must to be considered adequately in order to avoid misinterpretations.

Animals↗
PubMedDate not supplied

Dynamics of the hypertrophied left ventricle in the rat. Effects of physical training and chronic pressure load.

Left ventricular hypertrophy of about 40% was produced in rats by narrowing one renal artery (Goldblatt II) and of about 6% by swimming-training for 2 hours a day for 14 weeks. The dynamics of the hypertrophied ventricles were investigated by means of the isovolumic systolic and diastolic pressure-volume relations, the stress development during afterloaded and isovolumic contractions, and the force-velocity relation. The following results were obtained: The performance of the whole hypertrophied ventricle is increased. The developed stress and the maximum rate of stress development are enhanced, probably as a consequence of the increased density of the contractile proteins. The maximum shortening velocity can be reduced at the same time.

Adaptation, Physiological↗
PubMedDate not supplied

Ventricular pressure-volume relations as the primary basis for evaluation of cardiac mechanics. Return to Frank's diagram.

Considering ventricular function from the vantage point of the pressure-volume (P-V) diagram permits not only quantification of ventricular working capacity under normal and pathophysiological conditions but also promotes understanding of cardiac dynamics including prediction of the effects of mechanical and pharmacological interventions. Therefore it seems appropriate, at least intellectually, to classify all measured volume and pressure data into the scheme of the P-V diagram. The use of so-called contractility indices and also the restriction to the end-systolic P-V relation alone means deliberate renunciation of important information. In principle, Frank's original concept can be confirmed which, under afterloaded conditions, implies the existence of distinct end-systolic P-V curves each related to a particular end-diastolic volume. As an approximation, however, the assumption of one common end-systolic P-V relation seems tolerable. Based on Frank's diagram, a concept for assessment of ventricular and myocardial function is presented following a discussion of the determinants of the diastolic and end-systolic P-V relations, as well as the methodological difficulties and different notions with regard to the end-systolic P-V curve. The P-V area between the curves of systolic maxima and diastolic minima, up to a defined end-diastolic pressure, is recommended as a measure for quantitative evaluation of ventricular working capacity. Transformation into stress-length (sigma-l) relations is indispensable for assessment of myocardial function under the conditions of changed ventricular geometry. The normalized sigma-l area yields a measure for interindividual evaluation of myocardial working capacity. This concept of evaluation does not mean acknowledgement of the visco-elastic theory of muscle contraction nor of the Emax concept. The P-V and sigma-l relations must, however, be complemented by time related parameters in order to estimate ventricular and myocardial power capacity. After a long-lasting search through international literature for "contractility indices" of general applicability and significance it seems appropriate to return to Frank's diagram as the primary basis for evaluating cardiac mechanics.

Animals↗
PubMedDate not supplied

The effect of coronary perfusion pressure and preload on left ventricular systolic wall stress parameters.

The effect of coronary perfusion pressure (i.e., mean aortic pressure) and of left-ventricular preload (i.e., left-ventricular enddiastolic wall stress) on left-ventricular peak developed wall stress (sigma max) and the maximum rate of stress development (d sigma/dtmax syst) and relaxation (d sigma/dtmax diast) was examined in anesthetized rats under open-chest conditions. Pulmonary flow, aortic pressure, and left-ventricular pressure amplitude, as well as enddiastolic pressure and dP/dt were measured and the respective wall stress parameters were calculated from the measured pressure and volume data, assuming a thick-walled sphere. Aortic pressure and right-ventricular filling pressure could be adjusted independently of each other via two header tanks. A primary increase in coronary perfusion pressure results in a linear rise in sigma max, d sigma/dtmax syst, and d sigma/dtmax diast. With increasing preload, however, the systolic wall stress parameters only increase initially, run through a maximum and then decrease with further elevation of the leftventricular enddiastolic wall stress. These results are interpreted such that, at a given mean aortic pressure the wall stress developed in the left ventricle rises with increasing preload and, consequently, the difference between mean aortic pressure and mean left-ventricular intramural wall stress declines. With decreasing difference between mean aortic pressure and mean intramural wall stress, the coronary flow is reduced. This interplay between left-ventricular wall stress on the one hand and coronary flow on the other is expressed in the critical value of enddiastolic wall stress, at which a further increase in preload leads to a marked reduction in coronary flow and, hence, to a fall in the systolic wall stress parameters.

Animals↗