PubMed Health⌕ Search

Biomedical subjects

H Piene

Publications and source records attributed to H Piene.

At least 55 records · Page 3Linked to original sources
PubMed1984

Left ventricular diastolic relaxation and pressure-diameter relations during ischaemic left ventricular failure in the dog.

The significance of severe ischaemic left ventricular (LV) failure on the LV isovolumic relaxation process and diastolic chamber stiffness has been investigated in nine open-chest pentobarbital-anaesthetized dogs. LV failure was induced by bolus injections of 50 micron microspheres into left coronary vascular bed until LV minor axis diameter had increased about 25% and end-diastolic pressure about 20 mmHg. Such ischaemic LV failure did not shift the relation between diastolic LV pressure and minor axis diameter compared with pressure-diameter curves obtained before induction of failure. Neither inotropic nor chronotropic stimulation evoked such shifts. Assuming exponential pressure decline, LV relaxation was significantly slower during failure, but proceeded in all experimental conditions at rates which indicated complete relaxation in late diastole. Analysis of the pressure decline during LV relaxation demonstrated that this process proceeded faster than assumed by an exponential function both before and during LV failure.

Animals↗
PubMed1984

Left ventricle-aortic coupling: prediction of contraction pattern.

In control heart beats of six open-chest dogs we established a relationship between ventricular diameter and change in volume during systolic ejection, described ventricular mechanical performance by a time-dependent pressure-diameter relationship, and represented ventricular afterload in subsequent variably loaded test beats by aortic input impedance calculated from aortic flow and pressure. Impedance was manipulated by means of an inflatable balloon in the aorta. A computational procedure was developed which combined the independent and general descriptions of ventricle (1 and 2 above) and load (3 above) to predict the time course and mean values of aortic pressure, flow, ventricular pressure, and diameter over a broad range of aortic impedance. Predicted data were compared with those directly observed at identical impedance. High degree of accordance between predicted and observed data of stroke volume, mean aortic and mean ventricular pressure was found, but diameter shortening was less accurately predicted. Previously assessed dependency of the ventricular pressure-volume-time relationship on aortic flow and "ejection history" was also incorporated in the calculations. This caused improved prediction of the flow pulse configuration, but the quality of predictions of mean values of pressures and flow was not enhanced.

Animals↗
PubMed1984

Platelet trapping and haemodynamics in unilateral and bilateral experimental pulmonary macroembolism.

Cat lungs were embolized with autocoagulated autologous blood clots and the platelet-trapping ability of the lung vessels and the haemodynamic responses were studied. Embolization was bilateral or strictly unilateral. It elicited on average a twofold increase in 51Cr-labelled platelets in embolized parts of the lungs. Microscopy revealed platelet aggregates in arteries with diameter 50-100 microns. A temporary decrease in systemic platelets immediately postembolus was found. In the nonembolized lung at unilateral embolization the pulmonary platelet aggregation did not occur and no haemodynamic response was detected, indicating that platelet-aggregating substances or humoral factors did not recirculate from affected to unaffected parts of the lungs.

Animals↗
PubMed1983

Right ventricular mechanics: a comparison of models.

Using data from an isolated supported cat right ventricle preparation, we investigated the following models or methods for characterising the mechanical function of the ventricle: (1) a pressure generator in series with an internal impedance; (2) a variable elastance in series with an internal, pressure dependent flow resistance; (3) pulse response analyses, theoretically based on the pressure response to a small volume step of short duration; and (4) geometric mapping of the variables pressure and volume as functions of time. We tested the reproductive and predictive strengths of the four models, and found that all methods could reproduce 50% of the observed pressure curves with an RMS error less than 0.2 kPa, and in most cases also gave a close prediction of pressure curves which were not used to establish the respective model parameters. We see this as one reason for the fact that no single ventricular model has yet been universally accepted.

Animals↗
PubMed1983

Local auxotonic systolic force and work in canine right ventricular free wall.

Regional auxotonic force (F) and segment length (SL) were measured in the right ventricular (RV) free wall of 10 anesthetized dogs. F was obtained with a Feigl force gauge and SL with ultrasonic crystals positioned in the inflow or outflow region and in the longitudinal or transverse direction. Although the time courses of right ventricular pressure and force were almost identical, the timing of right ventricular ejection had little relationship to specific parts of the force-segment-length loop. Thus local F vs. SL loops were of irregular form signifying local lengthening or shortening in isovolumic periods. Local work, i.e., F vs. SL loop area, increased linearly with cardiac output (CO), which was varied by volume expansion or reduction. A predominant contribution to total RV work from any particular region and direction was not observed. A "local contribution factor" [eta, defined as (local work/local area)/(total RV work/free wall area)] fell with increased CO from 2.1 +/- 0.5 at 1.1 l/min to 0.7 +/- 0.2 at 4.8 l/min. This observation suggests that transformation of local into total work became more efficient at higher CO or that structures other than the free wall became increasingly important for RV pump function at higher output levels.

Animals↗
PubMed1982

Does normal pulmonary impedance constitute the optimum load for the right ventricle?

Right ventricular performance of isolated supported cat hearts was experimentally characterized by a relationship among ventricular pressure (P), volume (V), and time after onset of systole. This characterization was combined with a hypothetical load network consisting of lumped central and peripheral lung vascular resistances (Rc and Rp), inertance (L), and compliance (C). We calculated ventricular and load pressure, flow, external ventricular work (Wext), static ventricular P-V energy (Wstat), and pump efficiency Q = Wext/Wstat over a broad range of load conditions. Magnitudes of load network variables resulting in a maximum value of Q would define the load impedance matching the ventricle. A practical optimum magnitude of lumped vascular compliance was obtained at C = 150 x 10(-6) g-1 . cm4, above which no substantial change in Q took place. We obtained maximum Q at approximately 4 ml stroke volume (heart rate = 2 Hz) and at characteristic impedance between 0.75 and 1.1 x 10(3)g . cm-1 . s-1. As these values are quite close to those encountered in the intact animal, we conclude that the right ventricular and the pulmonary arterial tree appear to constitute a matched pump-load system.

Animals↗
PubMed1981

A force-length-time relationship describes the mechanics of canine left ventricular wall segments during auxotonic contractions.

We examined regional mechanics of the left ventricular free wall in naturally pumping dog hearts during beta-blockade. Local systolic wall force (F) and segment length (L) were obtained with an auxotonic force gauge and an ultrasonic dimension gauge, both inserted at the equatorial level of the wall to measure F and L in the circumferential direction. Shortening velocity (-dL/dt) was obtained by differentiation of L. Preload and afterload were changed by acute caval and/or aortic occlusion so that a wide variation in F, L, -dL/dt, and dF/dt during shortening was obtained. In all experiments, F vs. L at identical time (t) after end-diastole (ED) fell on well-defined lines, irrespective of the -dL/dt line (t = 200 msec) was equivalent to a drop of approximately 50% in F at 10% reduction in L. No defined relationship was observed between F, L, and -dL/dt. However, by superimposing F, L, and -dL/dt curves from contractions of high EDL and high -dL/dt on those from contractions of low EDL and low -dL/dt, and comparing F and -dL/dt at identical L and t, a slightly lower F (difference 2.23 +/- 1.09 g, P approximately 0.05) could be associated with the higher -dL/dt (difference 0.6 +/- 0.1 muscle length/sec, P less than 0.001). These data suggest that the F-L-t relationship is a valid descriptor of auxotonic contractions in the ventricular wall, and that the direct effect of shortening velocity on the wall force is modest.

Animals↗
PubMed1980

Performance of the right ventricle: a pressure plane analysis.

A load invariant presentation of the heart's ventricular performance has been investigated. Flow from the right ventricle of isolated cat hearts was passed through a controlled, variable load. Ventricular pressure and flow were recorded and ventricular volume computed by flow integration. The three-dimensional trajectories of ventricular pressure, ventricular volume and time after onset of contraction all closely followed a single three-dimensional surface, which was denoted as the PVt surface. The PVt surface depends on the inotropic condition of the heart, but is load invariant. It is therefore a measure of the intrinsic ventricular performance. Given the arterial load on the ventricle, it can be applied for predictions of pressure and flow profiles, as well as any parameter related to them.

Animals↗
PubMed1980

Interaction between the rigt heart ventricle and its arterial load: a quantitative solution.

Piene and Sund (Cardiovasc. Res., 1980) have recently demonstrated that the performance of the ventricle can be expressed by relating the principal variables pressure (P), volume (V), and time after onset of contraction (t): P = function (V,t). The function can be mapped experimentally as a three-dimensional surface, denoted the PVt surface, and can thereafter be approximated by an empirical equation. The vascular load of the ventricle is defined by the arterial input impedance vs. frequency graph, Z(f), which can be converted to the time domain by inverse Fourier transformation. This report describes how flow and pressure generated by the ventricle can be calculated when the independent expressions for the ventricle and for the load are given. The method is applied on right ventricular contractions of isolated cat hearts, and excellent fit between calculated and observed flow and pressure curves was obtained.

Animals↗
PubMed1979

Flow and power output of right ventricle facing load with variable input impedance.

The output from the right ventricle (RV) was studied at different load impedances. Isolated cat hearts were perfused with Tyrode solution with erythrocytes. Coronary perfusion pressure and RV end-diastolic pressure were kept constant. The RV pumped into an artificial hydraulic load with independently variable resistance (R) and compliance (C). Mean RV flow (RVO) decreased after R increase or C reduction. For each heart, RVO and mean RV pressure were linearly related. The slope of the regression line is interpreted as an "apparent source resistance" (Rs). Rs was on average 3.4 X 10(3) (dyn.s.cm-5). The static hydraulic power output was maximum at a certain load R (Rm). Rm was C dependent at an average high C of 5 X 10(-5) dyn-1.cm5, Rm was 9.4 X 10(3) dyn.s.cm-5 on average and shifted to 5.4 X 10(3) at low C (avg 0.8 X 10(-5). Theoretical considerations show that Rm/Rs will be equal to total heart period divided by ejection period in the extreme case C leads to infinity, and Rm/Rs leads to 1 when C leads to 0. Experimentally, Rm/Rs was 2.4 (avg) for high C, and approached 1 for low C, which fits the theoretical predictions. The results indicate that high C facilitates the matching between the right heart and the vascular resistance in the lung.

Animals↗
PubMed1976

Reduction of pulsatile hydraulic power in the pulmonary circultation caused by moderate vasoconstriction.

Vascular input impedance and associated hydraulic power was measured in rabbit isolated lungs. The study was focused on changes in impedance and in pulsatile hydraulic power during relaxation and contraction of vascular smooth muscle. Pulsatile power was found to be at a minimum when smooth muscle tone was such that the pulmonary arterial pressure was in the physiological range, and increased both when the vessels were relaxed and further constricted. Input impedance was found to be determined mainly by the large, proximal ('extra-alveolar') arteries.

Acetylcholine↗
PubMed1976

Influence of moderate vasoconstriction on the wave reflection properties of the pulmonary arterial bed.

Increased transmural pressure in the pulmonary arterial bed may reduce vascular input impedance and reduce hydraulic power linked to pulsatile blood flow. Vascular impedance and pulsatile hydraulic power (Wp) levels of isolated perfused rabbit lungs were compared after similar rises of pulmonary arterial pressure (PAp), induced either by vasoconstriction or by left atrial pressure (LAp) elevation. Resulting Wp levels were significantly smaller after vasoconstriction than LAp elevation. Wp showed a minimum level at physiologic PAp (about 20 cm H2O) irrespective of the cause of PAp elevation. Pressure pulse wave reflection coefficient (see article) was calculated for control and test situations, and was found to be approximately doubled after vasoconstriction. Only minor changes in (see article) were found after LAp elevation. Accordingly, moderate vasoconstriction (resulting PAp approximately 20 cm H2O) caused a backward traveling pressure wave of high amplitude, appearing in counter-phase to the forward pressure wave at the input site. The total pressure wave amplitude was thereby markedly lowered, resulting in a reduced Wp level. We assume that this effect of moderate vasoconstriction may be one reason for the existence of vascular smooth muscles in the pulmonary arteries.

Acetylcholine↗
PubMed1976

The influence of pulmonary blood flow rate on vascular input impedance and hydraulic power in the sympathetically and noradrenaline stimulated cat lung.

This study was designed to evaluate the influence of sympathetic nerve stimulation (SN) and alpha-adrenergic receptor stimulation (alphaS) on the pulmonary vascular input impedance and hydraulic power output of the right heart during variations of cardiac output (CO). An open chest cat preparation was used and pulsatile pressure and flow in the pulmonary artery were measured by high frequency response transducers. Calculations showed that vascular resistance (VR) was inversely dependent on CO, but input impedance of the unstimulated lung was not influenced by CO variations. NS or alphaS increased VR and input impedance significantly, and the relation pulsatile hydraulic power/total hydraulic power (Wp/Wt) increased 40%, indicating that such stimulation has larger relative influence on impedance than on resistance. The reduction of arterial compliance during NS (maximal stimulus) was calculated to be 60%, independent of CO. Input impedance during NS or alphaS was reduced by CO elevations, probably because the concomitant distension of the arterial bed reduced arterial resistance and inertance. The ratio Wp/CO, which expresses the fraction of pulsatile hydraulic power lost per ml mean arterial flow, was found to be flow dependent both in control and stimulated conditions: Wp/CO was positively correlated to CO in control condition and weakly negatively correlated to CO during stimulation. At high CO the arterial vessels could be stimulated and stiffened without much extra load on the right heart.

Animals↗
PubMed1976

Influence of vessel distension and myogenic tone on pulmonary arterial input impedance. A study using a computer model of rabbit lung.

A computer model of the pulmonary arterial (PA) bed of rabbit lungs was designed in order to test experimental observations of changes in PA input impedance and pulsatile hydraulic power (cap.) during increased PA pressure. The computer model was based on a simple 3-component analog representation of single vessels (i.e. resistance, inertance and compliance). 16 generations of arterial vessels, from PA to 60 mum diameter, were combined to calculate PA input impedance. Input impedance was found to mimic closely that observed experimentally. Both venous pressure elevation and arteriolar constriction was found to reduce input impedance and Wp. By combining arteriolar constriction with increased myogenic tone of the larger arteries, Wp was found to show a minimum level at a certain PA pressure, dependent on the degree of arterial stiffening. Wp was found to follow changes in arterial volume and resistance during stimulated vasoconstriction. Wp dissipation in arterial vessels was calculated to approx. 50% of total imput Wp at physiological pressure conditions, and could be reduced by one half after PA pressure increase from 20 to 50 cm H2O, despite a concurrent halving of arterial compliance. Arterial vessels smaller than 200 mum diameter were found to have negligible direct influence on PA input impedance.

Animals↗