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Biomedical subjects

P Krösl

Publications and source records attributed to P Krösl.

At least 19 recordsLinked to original sources
PubMed2001

Beat-to-beat evaluation of cardiac function in low-dose endotoxemia using a conscious sheep model.

The effects of very low doses of endotoxin (20 ng/kg/h for 8 h) were evaluated in a conscious sheep model in which introducers for catheters for monitoring pressure and ventricular dimensions had been previously inserted so that the studies could be performed without anesthesia and without a previous thoracotomy. Analog data was obtained at hourly intervals for 10 h and again at 24 h and was used to construct a beat-to-beat analysis of left ventricular performance. Only minimal effects were observed on heart rate, end diastolic pressure, arterial pressure, cardiac output, or cardiac work, although there was a significant rise in pulmonary artery pressure at 1 h of infusion. Despite the absence of changes in heart rate, preload, or afterload, maximal dp/dt decreased significantly by 4 h and remained decreased for the 10-h observation period; it returned to normal at 24 h. End systolic elastance decreased at 6 h and Pmax/EDV, a new indicator of performance, also decreased at 6 and 9 h. Thus, systolic performance decreased. Negative dp/dt did not change, but time for relaxation from 80% to 20% of peak ventricular pressure increased significantly at 5, 6, and 8 h. Plasma TNF-alpha was also measured and showed a significant rise at 2 h, but rapidly decreased thereafter. These results indicate an early depression of myocardial contractility and distensibility at doses of endotoxin insufficient to produce measurable effects on arterial pressure or cardiac output.

Animals↗
PubMed1998

Problems with use of the end systolic pressure-volume slope as an indicator of left ventricular contractility: an alternate method.

The use of end-systolic elastance as a parameter of left ventricular contractility is based on a theory put forward by Sagawa and is limited by an assumed linearity of the model for a time varying compliance. A major problem is the contractility-dependent curvilinearity of the end-systolic pressure-volume relationship (ESPVR), which may result in intercept volumes that are below a passive unstretched volume. Based on the experimental data of Burkhoff et al., we demonstrate the reasons for the lack of correlation of the slope (k) of the end-systolic pressure (P(es))-volume (V(es)) relationship with ventricular contractility. A parabolic relation, P(es) = a x V(es)2 + b x V(es) + c, was used for approximation of the ESPVRs, as proposed by Burkhoff et al., and the slope (k = 2 x a x V(es) + b), together with the volume axis intercepts (V0), calculated for the tangents for all P(es)/V(es) points of the ESPVRs. The results demonstrate the volume range dependence of the slope and V0 of linear regression lines. However, intercepts of the ESPVRs tangents with a midrange constant pressure line (e.g., 80 mmHg or 100 mmHg) justify the use of the shift of the end-systolic pressure-volume relationship as a parameter of left ventricular contractility. This method appears to be valid over a much wider range of end-systolic volumes than is the use of the slope alone.

Animals↗
PubMed1998

Left ventricular potential energy is represented in the ejecting left ventricular pressure curve.

Sunagawa and coworkers have proposed an ejecting, single beat, cosine curve matching method for the estimation of the maximum potential left ventricular pressure during an isovolumic contraction. We tested the hypothesis that this same information could be obtained from maximum dp/dt and the length of the ventricular contraction curve using a simple formula. The method was tested using Sunagawa's reported data as well as on data obtained from five dogs over a wide range of afterloads, and from three rabbits, four pigs, and four sheep. A high correlation coefficient between the two methods (.85 to .97), based on a linear model, was obtained in all the experiments. The formula method gave slightly higher values than the cosine curve matching procedure, was much simpler, and involved few of the curve matching assumptions. The maximum left ventricular pressure was also highly correlated with stroke work. These results imply that the maximum potential left ventricular pressure or energy is represented in, and can be predicted from, the ventricular pressure during normal ejection at a given end diastolic volume. When combined with measurements of end systolic pressure and stroke volume, reliable beat-to-beat estimates of the slope of the end systolic pressure-volume relationship (end systolic elastance) might be obtainable from single, left ventricular beats.

Algorithms↗
PubMed1994

Myocardial function in septic sheep.

There is an ongoing discussion whether the heart is the primary target organ responsible for the development of cardiovascular failure during septic shock as well as its onset. We tried to study the reaction of the heart to sepsis in the early phase of 8 h, using a sublethal model of sepsis in six awake cross-bred Austrian mountain sheep. Sepsis was induced by infusion of a live Escherichia coli suspension at a dose of 5 x 10(7) colony-forming units per kg body weight over 8 h. Standard hemodynamic, hematologic and serum tumor necrosis factor (TNF) measurements were obtained. For evaluation of left ventricular performance we used the following methods, tested in five pilot experiments: 1) The shift of the end-systolic pressure-diameter relation. This was characterized by the calculated shift of the transverse external end-systolic diameter of the left ventricle at a "midrange" end-systolic pressure of 100 mmHg (end-systolic ventricular diameter deviation, ESVDD100). Calculations were performed using a second order regression function of the end-systolic pressure diameter points obtained by variation of afterload by a cuff occluder on the aorta; 2) The shift of the (dP/dt)max over end-diastolic diameter ratio compared to control values estimated by a graphical approach. Mean pulmonary pressure increased from 21 +/- 1 to 36 +/- 2 mmHg in the first hour after starting the E. coli infusion and remained elevated during the entire 8 h observation period. Serum TNF was found to peak 1 hour after start of E. coli infusion and was hardly detectable after 3 hours of bacteremia. Mean aortic pressure showed minor changes (maximum 105 +/- 3 mmHg, minimum 91 +/- 2 mmHg) and there were no statistically significant alterations of the cardiac index. ESVDD100 showed an "oscillatory" reaction in the first phase and a statistically significant decrease of contractility in the second phase (at 4 h). This was confirmed by the graphical method of the (dP/dt)max over end-diastolic diameter ratio. We may therefore conclude that there is no early depression of myocardial function or if so, it may be masked by adrenergic stimulation. In the later phase of the 8 h experiment there is a significantly decreased contractility of the heart. This may be compensated (e.g., "Starling" mechanism or heart rate increase) in this sublethal model.

Animals↗
PubMed1989

Permeability studies in a hypovolemic traumatic shock model: comparison of Ringer's lactate and albumin as volume replacement fluids.

In order to shed light on the controversy surrounding the choice of resuscitative fluids in shock, we used a canine model which we feel to be a superior mimic of human traumatic shock, combining hemorrhage (to a mean arterial pressure of 50 mmHg), fracture of both femora, and soft tissue crush. After 90 min, animals were resuscitated by reinfusion of shed blood, supplemented by 5% albumin (n = 8) or lactated Ringer's solution (n = 8). Plasma colloid osmotic pressure (COP), transcapillary escape rate for albumin (TER), total lung water and extravascular lung water (EVLW) were measured. COP fell in both groups, but remained above 9 mmHg in the albumin recipients, while falling below 7 in those receiving crystalloid (P less than 0.05). Overall, the increase in EVLW averaged 20%; albumin recipients fared better (9.7%) than Ringer's recipients (31.1%), but wide inter-animal variation precluded statistical significance (P = 0.095). TER rose 30% per hour, without difference between groups. Quality of resuscitation (achieved blood pressure and cardiac output) was somewhat better in the albumin group. We conclude that this model allows study of the early microvascular leakage seen in shock; within the time-frame studied (maximum 4.5 h following shock), colloid and crystalloid resuscitation were approximately equivalent.

Albumins↗
PubMed1988

Control of perfusion pressure and flow in isolated heart bioassays.

Bioassays using isolated animal hearts are important tools for the investigation of cardiac behaviour, but to obtain accurate results a proper perfusion circuit has to be designed. In particular, biophysical studies of contractile and vascular behaviour require a perfusion circuit which permits the adjustment of several experimental parameters within wide ranges. It must also be able to maintain the stability of these parameters when the behaviour of the isolated organ undergoes major changes. To meet this requirement, we have developed a perfusion circuit which makes it possible to control either the perfusion pressure or the coronary flow, with a high degree of precision. There is an electronic controller which satisfies the requirements of a variety of safety and experimental requirements and guarantees a well-defined perfusion system. Computer simulation of the interaction between the perfusion circuit and the heart identified the basic elements of this time-variable, nonlinear system.

Animals↗
PubMed1983

Importance of myocardial loading conditions in determining the effects of enflurane on left ventricular function in the intact and isolated canine heart.

The effect of enflurane (2% and 4% inspired) on left ventricular (LV) function were examined in chronically instrumented dogs, both intact and after isolation of their hearts and lungs from the systemic circulation. Enflurane in the intact dogs increased heart rate (32 +/- 5% with 2% and 41 +/- 4% with 4%) and elicited striking, dose-dependent decreases in LV stroke shortening (-30 +/- 3% and -41 +/- 4%), the maximum velocity of LV fiber shortening, dD/dt, (-23 +/- 2%) and -40 +/- 2%), LV systolic pressure (-25 +/- 3% and -33 +/- 2%), the maximum rise of LV-pressure, dP/dt (-33 +/- 5% and -55 +/- 3%), and mean aortic pressure (-27 +/- 2% and -37 +/- 1%). However, the LV diastolic performance was impaired little, i.e., even with the higher concentration the LV end-diastolic pressure rose only moderately (32 +/- 4%), while the LV end-diastolic dimensions failed to change significantly; both LV end-diastolic pressure and LV end-diastolic diameter were decreased with the low concentration. Enflurane, after beta-adrenergic blockade alone or after combined beta-adrenergic and cholinergic blockades, or with spontaneous ventilation instead of controlled ventilation, had similar effects. By contrast, in the hearts that were isolated from the systemic circulation and the complex neurohumoral environment, enflurane increased both LV end-diastolic pressure (116 +/- 32% and 492 +/- 58%) and LV end-diastolic diameter (13 +/- 3% and 28 +/- 7%). In intact dogs with aortic pressure artificially increased to conscious control levels, enflurane likewise caused a distinct depression of the LV diastolic performance. Thus, LV systolic unloading appears to be mandatory in order to prevent acute myocardial failure from higher doses of enflurane. The observed changes in LV function with enflurane are largely independent of cardiac rate, adrenergic and cholinergic influences, and the hemodynamic consequences of intermittent positive-pressure ventilation.

Animals↗
PubMed1978

[Physical fundamentals of pressure measurement (author's transl)].

The important role of pressure-measurement for many diagnostic, surgical, critical care and biomedical research problems should not be underestimated. For high accurancy the good knowledge of the underlying physical and mathematical principles seems to be necessary. On the other hand many users need some quick and easy methods for units of pressure measurements testing and calibration of their pressure-measurements system. In this survey a small introduction to the units is followed by basic considerations about fluid-mechanics. Fourier-analysis and theory of transmission. (The influence of terms like "natural frequency", "damping" and "phase lag" are shown). After the description of the commonly used pressure-transducers some hints are given to check the systems even in small laboratories.

Manometry↗