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Biomedical subjects

G Kissling

Publications and source records attributed to G Kissling.

67 records · Page 4Linked to original sources
PubMedDate not supplied

Geometric and muscle physiological factors of the Frank-Starling mechanisms.

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

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

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↗
PubMedDate not supplied

Left ventricular end-systolic pressure-volume relationships as a measure of ventricular performance.

The extent to which conclusions about myocardial performance may be drawn from end-systolic pressure-volume relations was investigated. Left ventricular isovolumetric and end-systolic pressure-volume relationships were measured in the rat, under acute impairment of contractility (hexobarbital), at chronic pressure overload (spontaneously hypertensive rats), and at chronic volume overload (aorto-caval shunt). Our results confirm the classic conception of Otto Frank where the curves of the isovolumetric maxima and the curves of the end-systolic pressure-volume relations follow separate courses. Acute alterations in contractility can be detected from shifts in the end-systolic pressure-volume relations. In chronic pressure or volume overloaded hearts the end-systolic pressure-volume relations do not render conclusions about ventricular or myocardial performance since in chronically altered hearts, the course of the end-systolic pressure-volume relations is primarily influenced by geometric factors.

Animals↗
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

Alterations in cardiac oxygen consumption under chronic pressure overload. Significance of the isoenzyme pattern of myosin.

Hypertension and resulting left ventricular hypertrophy was induced in young male Wistar rats (60 to 70 days old) by narrowing of one renal artery (Goldblatt II). 8 and 24 weeks after operation, myocardial oxygen consumption was measured on a modified in situ heart-lung preparation with nearly isovolumetric left ventricular contractions. Measured myocardial oxygen consumption was related to left ventricular wall stress. The myosin isoenzyme pattern of each heart was determined with pyrophosphate gel electrophoresis. Oxygen consumption related to wall stress averaged over the entire heart cycle amounted to 15 mumoles O2/g X min 8 weeks after operation, and 24.4 mumoles O2/g X min in age-matched controls (delta 38%, p less than 0.0005). When wall stress was averaged over systole, oxygen consumption of the hypertrophied hearts amounted to 0.112 mumoles O2/g x beat, and 0.149 mumoles O2/g x beat in the controls (delta 25%, p less than 0.05). The proportion of VM-3 (the cardiac myosin isoenzyme of lowest ATPase activity) increased from 26.3% in the controls to 30.1% in the Goldblatt hearts (delta 14%, n.s.). 24 weeks after operation, oxygen consumption related to wall stress averaged over the entire heart cycle amounted to 16.1 mumoles O2/g x min, in age-matched controls 20.5 mumoles O2/g x min (delta 21%, p less than 0.05). When wall stress was averaged over systole, oxygen consumption of the Goldblatt hearts amounted to 0.080 mumoles O2/g x beat, and in the controls 0.107 mumoles O2/g x beat (delta 25%, p less than 0.0005). The proportion of VM-3 increased from 33.5% in the controls to 43.2% in the hypertrophied hearts (delta 29%, p less than 0.05). The present findings indicate that the reduced oxygen consumption of the pressure-loaded heart should be attributed to a redistribution of myosin isoenzymes. The transformation of myocardium into a slower, but more efficiently working muscle due to an increase in VM-3 can be interpreted as an adaptational process.

Animals↗
PubMedDate not supplied

Oxygen consumption and substrate uptake of the hypertrophied rat heart in situ.

A new heart preparation was developed which permits in situ measurements of myocardial oxygen consumption and substrate uptake in small animals. Using the new method the mechanical activity, as well as oxygen consumption and substrate uptake of the heart, was measured in Goldblatt rats with left ventricular hypertrophy of about 40%. 1. In agreement with former investigations on the hypertrophied rat heart, this model also shows that both the performance of the whole ventricle, as well as the contractile force per unit of cross-sectional area, is increased in the state of stable hypertrophy. 2. The absolute values of oxygen consumption and substrate uptake are increased in the hypertrophied hearts. However, oxygen consumption and substrate uptake as related to muscle mass and to wall stress were largely identical in hypertrophied and control hearts. 3. Hypertrophied hearts and controls utilize substrates according to their respective arterial blood concentration. Under our experimental conditions approximately 50% of the total energy in both groups is obtained from glucose, 30% from lactate, and 20% from fat. The relatively high consumption of lactate could be explained by the glucose uptake and lactate release of the erythrocytes.

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↗
PubMedDate not supplied

Predicting success for baccalaureate graduates on the NCLEX-RN.

The purpose of this retrospective study was to identify predictors of success for baccalaureate nursing graduates on the National Council Licensure Examination-Registered Nurse (NCLEX-RN). Subjects (505) were graduates of a baccalaureate nursing program in the southeastern United States from 1993 to 1998. The outcome variable was pass/fail on the NCLEX-RN on the first attempt. Predictor variables included type of student (freshman admission, transfer, second degree), age at the time of licensing examination, gender, performance on selected prenursing courses, performance in all junior and senior nursing courses, cumulative grade point average (GPA) at graduation and the Mosby AssessTest score. Results showed a significant relationship between number of Cs, Ds, and Fs in nursing courses and NCLEX-RN results. Students who passed the NCLEX-RN had significantly higher average GPAs, made fewer grades of C or below, and scored higher on the Mosby AssessTest than students who failed. Nontraditional college-age students tended to have a higher passing rate than did traditional age students. A logistic regression model was developed that correctly predicted 76 per cent of the students who failed based on the information available by the end of the end of the first semester of the senior year. J Prof Nurs 17:121-127, 2001.

Adult↗