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Biomedical subjects

G Kissling

Publications and source records attributed to G Kissling.

At least 19 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↗
PubMed1988

Haemodynamic effects of amrinone in the anaesthetized pig.

The vasodilator and inotropic actions of amrinone were investigated in mini-pigs under pentobarbitone anaesthesia. Left ventricular volume was determined angiocardiographically under afterload and isovolumetric conditions. Furthermore, aortic flow, left ventricular pressure and aortic pressure were measured. In some of the animals, the beta-adrenergic receptors were blocked with propranolol prior to the administration of amrinone. Without blockade of the beta-receptors, amrinone (2 mg kg-1) caused a significant reduction in mean aortic pressure. Due to less end-diastolic ventricular filling, stroke volume decreased, and thus ejection fraction remained constant. Since heart rate increased under amrinone, cardiac output remained constant. At the same time, the maximum rate of pressure rise increased, despite less end-diastolic ventricular filling. After blockade of the beta-adrenergic receptors, aortic pressure, end-diastolic ventricular filling, and stroke volume also decreased with amrinone. In contrast, heart rate remained practically constant, so that cardiac output declined. The maximum rate of pressure rise also declined due to less end-diastolic ventricular filling. It can be concluded from these results that, in situ, the primary action of amrinone occurs on vascular smooth muscle and that a positive inotropic activity with a normal dosage of amrinone is only an indirect outcome of reflex activation of the sympathetic system. Analysis of isovolumetric mechanograms and the ejection phase does not indicate a direct positive inotropic effect of amrinone. In the failing heart, however, beneficial effects can be expected, since the maxima curves follow a flatter course. Thus a reduction in afterload can lead to a significant increase in stroke volume, provided that aortic pressure does not fall below the critical coronary perfusion pressure.

Amrinone↗
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↗
PubMed1987

Ultrasonic recognition of the small-for-gestational-age fetus.

Sonar biparietal diameter, femur length, abdominal circumference, femur length/abdominal circumference ratio, ponderal index, and estimated fetal weight were obtained within ten days of delivery of small-for-gestational-age (SGA) (N = 102) and non-SGA (N = 204) newborns. The effectiveness of each ultrasound variable in the antenatal recognition of the SGA fetus was assessed. An abnormal abdominal circumference was the best predictor, confirming SGA in 98% of cases. Other variables (biparietal diameter, femur length, femur length/abdominal circumference ratio, ponderal index, or estimated fetal weight) were less accurate for predicting SGA. When we determined expected results based on a 10% prevalence of SGA, negative predictive value was greater than 92% for all variables studied; however, with the exception of estimated fetal weight and femur length, positive predictive values were disappointing, including abdominal circumference (21%). This report establishes the limits of ultrasound-derived growth variables in the antenatal identification of the SGA fetus.

Birth Weight↗
PubMed1986

The influence of myosin isoenzyme pattern on increase in myocardial oxygen consumption induced by catecholamines.

Investigations were performed in a modified heart-lung preparation of the rat in situ to ascertain to what extent the myosin isoenzyme pattern affects the catecholamine-induced increase in myocardial oxygen consumption. Accordingly, the myocardial oxygen consumption was measured in young Wistar rats with mostly VM-1 myosin and older spontaneously hypertensive rats with mostly VM-3 myosin, both under control conditions and after 0.05 mg/kg orciprenaline. In the controls (73.7 +/- 3.35% VM-1) the oxygen consumption related to TTI increased from 0.098 +/- 0.003 to 0.129 +/- 0.004 microM O2/g X beat under orciprenaline (+32%, p less than 0.005). In the SHR (27.8 +/- 0.58% VM-1) there was no significant increase in O2-consumption related to TTI (control conditions 0.093 +/- 0.003; orciprenaline 0.095 +/- 0.004 microM O2/g X beat; +2%, n.s.). Our investigations demonstrate that the degree of catecholamine-induced increase in myocardial O2-consumption depends on the isoenzyme pattern of myosin.

Animals↗
PubMed1985

Characteristics of the plaque under a coronary thrombus.

Young men dying suddenly and autopsied by the coroner sometimes have coronary thrombosis at a relatively early stage of arteriosclerosis. The plaques under such thrombi often have a complex of features, a) rupture, b) hemorrhage, c) medial destruction, d) nodular collections of foam cells, e) calcification, f) cellular infiltrates of the fibrous cap, fibrous base and adventitia, and g) a newly described kind of phagocytic activity at the boundary between the necrotic core and the fibrous base of the plaque. Commonplace innocuous plaques in most middle and old aged subjects without heart disease also often have some of these features. What structural characteristics might distinguish rare thrombogenic from commonplace innocuous plaques? Twenty-one thrombotic plaques from 18 cases of sudden coronary heart disease (CHD) death were histologically compared with 129 nonthrombotic plaques from these same 18 cases, 85 plaques from 23 cases of CHD death due to arteriosclerotic occlusion, and 94 plaques from 22 cases having no CHD. Plaques with thrombosis all had necrotic cores; plaques for comparison with these were therefore chosen all to have necrotic cores. Rupture and hemorrhage were found in 90% of thrombotic plaques, with mixing of plaque gruel and blood in the thrombus. Medial destruction, foam cells and calcification (features c, d, and e) were commonplace in all types of plaques. Small-cell infiltrates and atherophagocytosis (features f or g) were found in 72-94% of the 21 thrombotic plaques, but only in 18-24% of the 94 not CHD plaques. The necrotic core, characterized by crystalline cholesterol, appears to incite cellular responses in some plaques but not others; those responses distinguish thrombogenesis. The findings imply that thrombogenicity and its accompanying plaque cellularity are incited not by cholesterol, but by some trace or minor component of the plaque gruel of the necrotic core. The possibility of testing these hypotheses by practical methods has been shown to be feasible.

Aged↗
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↗