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Biomedical subjects

F W Prinzen

Publications and source records attributed to F W Prinzen.

At least 55 records · Page 3Linked to original sources
PubMed1993

Subepicardial fiber strain and stress as related to left ventricular pressure and volume.

In a mathematical model of the mechanics of the left ventricle (LV) by Arts et al. (1), assuming uniformity of fiber stress (sigma f) and fiber strain (delta epsilon f) in the wall during the ejection phase, fiber stress and fiber strain were related to LV cavity pressure (Plv), LV cavity volume (Vlv) and wall volume (Vw) by the following pair of equations: sigma f = Plv (1 + 3 Vlv/Vw) and delta epsilon f = 1/3 delta ln (1 + 3 Vlv/Vw). The ratio of Vlv to Vw appeared to be the most important geometric parameter, whereas the actual LV shape was of minor importance. The relationships on fiber strain and stress were evaluated experimentally in six anesthetized open-chest dogs during normal and elevated (volume loading) end-diastolic LV pressure. Subepicardial fiber strain was measured simultaneously in 16 adjacent regions of the LV anterior wall, using optical markers that were attached to the epicardial surface and recorded on video. Changes in Vlv were measured by use of four inductive coils sutured to the LV in a tetrahedric configuration. Vw was measured postmortem. During control as well as hypervolemia the following results were found. At the anterior free wall of the LV, the slope of the estimated linear relationship between measured and calculated fiber strain was 1.017 +/- 0.168 (means +/- SD), which is not significantly different from unity. Calculated fiber stress corresponded qualitatively and quantitatively with experimental results reported on isolated cardiac muscle. Calculated subepicardial contractile work per unit of tissue volume was not significantly different from global pump work as normalized to Vw. These findings support the assumption of homogeneity of muscle fiber strain and stress in the left ventricular wall during the ejection phase. Furthermore, average values of fiber stress and strain can be estimated on the basis of measured left ventricular pressure and volume.

Animals↗
PubMed1992

The time sequence of electrical and mechanical activation during spontaneous beating and ectopic stimulation.

The relation between the sequence of electrical (E) and mechanical (M) activation was studied at the LV anterior wall of open-chest dogs (n = 11). M activation was defined as the onset of epicardial fibre shortening, as measured with a recently developed video technique. E activation was determined with a brush of extracellular electrodes. The delay between activation of basal and apical regions was consistently larger for M activation than for E activation: during spontaneous beating: 20.5 +/- 7.30 ms vs 8.8 +/- 3.31 ms, during right ventricular outflow tract pacing: 50.3 +/- 7.69 ms vs 39.0 +/- 5.31 ms and during left ventricular apex pacing 40.1 +/- 10.03 ms vs 25.4 +/- 9.30 ms, respectively (P less than 0.05 in all cases). The E-M time interval was consistently shorter in early than in late activated regions: 32 +/- 10 vs 41 +/- 8 ms during RV outflow tract pacing (P = 0.09) and 24 +/- 30 vs 40 +/- 24 ms during LV apex pacing (P less than 0.05). Electrical asynchronies larger than 40 ms resulted in decreases of systolic blood pressure and stroke volume. This study shows that the asynchrony of cardiac motion exceeds that of electrical activation because the time interval between electrical activation and onset of fibre shortening is larger the later a particular region is activated. Possible explanations for this phenomenon are discussed.

Animals↗
PubMed1991

Mapping the sequence of contraction of the canine left ventricle.

A method has been developed to map the sequence of contraction as measured at the epicardial surface of the anterior free wall of the canine left ventricle during sinus rhythm and electrical stimulation of the ventricle. In an area of 35 x 45 mm, 40-60 white markers were attached to the epicardial surface. The motion of the markers was recorded on video and analysed off-line by computer. In an array of 35 regions, regional surface deformation and epicardial fibre strain were calculated from the motion of the markers. Between all adjacent regions, the differences in timing of contraction were determined by cross-correlation of the related fibre strain signals. A map of the time sequence of contraction has been calculated so that the sum of the squares of the deviations between time intervals of the map and the measurements was minimised. If individual correlation coefficients were found to be less than 0.85, the related time difference was discarded from the analysis. If more than 25% of the time differences were discarded because of this reason, the whole map was obtained by determining time of the negative peak of the second time derivative in the early phase of contraction. The accuracy in time marking was sufficient (+/- 7 ms), as compared to the time differences over the epicardial surface, which were found to be on the average between 10 and 80 ms in case of sinus rhythm and electrical stimulation of the right ventricular outflow tract, respectively.

Animals↗
PubMed1991

Relation between left ventricular cavity pressure and volume and systolic fiber stress and strain in the wall.

Pumping power as delivered by the heart is generated by the cells in the myocardial wall. In the present model study global left-ventricular pump function as expressed in terms of cavity pressure and volume is related to local wall tissue function as expressed in terms of myocardial fiber stress and strain. On the basis of earlier studies in our laboratory, it may be concluded that in the normal left ventricle muscle fiber stress and strain are homogeneously distributed. So, fiber stress and strain may be approximated by single values, being valid for the whole wall. When assuming rotational symmetry and homogeneity of mechanical load in the wall, the dimensionless ratio of muscle fiber stress (sigma f) to left-ventricular pressure (Plv) appears to depend mainly on the dimensionless ratio of cavity volume (Vlv) to wall volume (Vw) and is quite independent of other geometric parameters. A good (+/- 10%) and simple approximation of this relation is sigma f/Plv = 1 + 3 Vlv/Vw. Natural fiber strain is defined by ef = In (lf/lf,ref), where lf,ref indicates fiber length (lf) in a reference situation. Using the principle of conservation of energy for a change in ef, it holds delta ef = (1/3)delta In (1 + 3Vlv/Vw).

Animals↗
PubMed1990

Redistribution of myocardial fiber strain and blood flow by asynchronous activation.

Hearts of 11 anesthetized open-chest dogs were paced from the right atrium (RA), right ventricular outflow tract (RVOT), and left ventricular apex (LVA). Maps of the sequence of electrical activation (192 electrodes), fiber strain (video technique), and blood flow (microsphere technique) in the epicardial layers were obtained from a 15- to 20-cm2 area of the anterior left ventricular wall. Electrical asynchrony in this area was 10 +/- 5 (RA), 52 +/- 12 (RVOT), and 30 +/- 16 ms (LVA, mean +/- SD, P less than 0.05 for RVOT and LVA compared with RA). Epicardial fiber strain during the ejection phase was uniformly distributed during RA pacing. However, during ventricular pacing it ranged from 13 +/- 33% (RVOT) and 23 +/- 29% (LVA) of the value during RA pacing in early-activated regions to 268 +/- 127% (RVOT) and 250 +/- 130% (LVA) of this value in late-activated regions. Epicardial blood flow ranged from 81 +/- 22% (RVOT) and 79 +/- 23% (LVA) in early-activated regions to 142 +/- 42% (RVOT) and 126 +/- 22% (LVA) in late activated regions. In all above values P less than 0.05 compared with RA. During RVOT pacing, gradients of epicardial electrical activation time, fiber strain, and blood flow pointed in the same direction. Compared with RVOT pacing, during LVA pacing all gradients were opposite in direction, and the gradients of electrical activation time and blood flow appeared to be smaller. These results indicate that timing of electrical activation is an important determinant for the distribution of fiber strain and blood flow in the left ventricular wall.

Animals↗
PubMed1989

Discrepancies between myocardial blood flow and fiber shortening in the ischemic border zone as assessed with video mapping of epicardial deformation.

Myocardial function around the border of ischemia was investigated in eight open-chest dogs using video mapping of epicardial deformation. With this method, 40-60 white markers attached to the left ventricular epicardium were traced in time automatically. Before and 5-10 min after coronary artery occlusion, blood flow and epicardial deformation were determined in 30-40 regions with a spatial resolution of about 5 mm. Epicardial deformation was expressed as subepicardial fiber shortening and surface area decrease during the ejection phase. The latter indicates local contribution to stroke volume. The absolute values of these variables were normalized relative to the central ischemic (= 0%) and remote non-ischemic area (= 100%). The 50% contour line of a variable was defined as its border. The average distance between the borders of perfusion and function was not significantly different from zero, due to considerable variation in this distance both within one heart (+/- 5.7 mm) and between mean distances for different hearts (+/- 4.4 mm). The width of the transition zone (distance between the 20% and 80% contour lines) of surface area decrease and subepicardial fiber shortening was significantly larger (20.5 and 15.0 mm, respectively) than those of transmural and subepicardial blood flow (8.5 and 9.5 mm, respectively). The present results demonstrate that in a 20-mm zone around the border of ischemia, major discrepancies are present between perfusion and deformation.

Animals↗
PubMed1989

Liver blood flow measurement in the rat. The electromagnetic versus the microsphere and the clearance methods.

This study describes the simultaneous measurement of hepatic arterial and portal venous blood flow in the pentobarbital anesthetized rat by means of electromagnetic flowmeters. Hepatic arterial flow was 0.21 +/- 0.02 mL/min/g liver, and portal venous flow was 1.53 +/- 0.19 mL/min/g liver (n = 20). Flows remained stable for more than 3 hr. A clear advantage of the electromagnetic technique is that it allows the continuous simultaneous separate measurement of hepatic arterial and portal venous blood flow. Simultaneous measurement of hepatic blood flow by the electromagnetic method and the microsphere method yielded almost identical results. Adenosine infusion (100 micrograms/min) did not affect hepatic blood flow measured electromagnetically nor via the microsphere technique. The suitability of indocyanine green (ICG) as an indicator of hepatic blood flow was evaluated by comparing the ICG clearance at steady-state conditions to the values of liver flow obtained by direct electromagnetic measurement. ICG clearance was only 30% of the electromagnetically measured blood flow. These data strongly suggest that ICG clearance does not reflect liver flow in the rat. Intravenous infusion of the vasoactive agents phenylephrine (2, 4, 10 micrograms/min during 5 min) and adenosine (20, 40, 200 micrograms/min) did not affect portal venous nor hepatic arterial flow, measured by the electromagnetic method, although brisk effects on mean arterial blood pressure were observed. This suggests autoregulatory responses of the hepatic vascular bed. The data suggest that electromagnetic flowmeters may be used to measure portal venous and hepatic arterial flow simultaneously in anesthetized rats. The continuous measurement of both flows simultaneously offers a clear advantage over other methods of hepatic flow measurement.

Adenosine↗
PubMed1987

Accumulation of lipids and lipid-intermediates in the heart during ischaemia.

The content of non-esterified fatty acids (NEFA) and their CoA and carnitine esters is low in normoxic cardiac tissue. The majority of fatty acids is esterified in the triacylglycerol and phosphoglyceride pool. During myocardial ischaemia beta-oxidation of fatty acids is inhibited. In addition, turnover of the esterified fatty acid pools is most likely disturbed. Accumulation of hydroxy fatty acids, acylCoA and acylcarnitine rapidly occurs after the onset of ischaemia. The accumulation of NEFA is a slower process. In addition to extracellular sources, NEFA originate also from intracellular lipid pools, most likely from phosphoglycerides. Although it has been suggested that activation of phospholipase A2 occurs in ischaemic tissue, the mechanism underlying the enhanced degradation of phosphoglycerides ist still incompletely understood.

Acyl Coenzyme A↗
PubMed1986

The effect of diltiazem on myocardial recovery after regional ischemia in dogs.

The effect of diltiazem on post-ischemic metabolic and functional recovery was investigated in regionally ischemic dog hearts. The duration of ischemia was 60 min, followed by 60 min of reperfusion. Diltiazem (bolus injection of 0.1 mg X kg-1 body weight prior to ischemia, followed by a continuous infusion of 0.1 mg X kg-1 X h-1) had no effect on residual coronary flow in the centre of the ischemic area, but blunted the reactive hyperemia response after restoration of flow. The drug partially prevented the depletion of ATP and glycogen in the severely underperfused subendocardial layers, i.e. when residual flow was below 0.1 ml X min-1 X g-1. Reduction of the content of these substances in the subepicardial layers was moderate and not influenced by diltiazem. Segment shortening in the subepicardial layers disappeared whereas segment lengthening was observed in the subendocardial layers during the ischemic period. Diltiazem did not prevent the loss of contractile function. Despite an initial restoration of contractile function within 10 min after reperfusion, no significant beneficial effect of diltiazem treatment on mechanical function of the reperfused area was present thereafter.

Adenosine Triphosphate↗
PubMed1986

Mapping of epicardial deformation using a video processing technique.

A method has been developed to measure deformation of the canine epicardium during the cardiac cycle simultaneously in a number (eight) of small regions (1 X 1 cm2). Approximately 50 white markers (diameter 1.5 mm) are attached to the epicardium and their motion is recorded on tape by a video camera. Marker positions are detected by computer processing of the digitized images. In each region the three deformation parameters are calculated from the displacements of all markers in that region by means of a least-squares criterium. In the experimental situation in the center of the area of the epicardium analyzed the accuracy of measuring circumferential strain, base-to-apex strain and shear is +/- 0.005, +/- 0.005 and +/- 0.002 rad, respectively. The method has been applied in an experiment in which local ischemia of the left ventricular wall was induced by occluding the anterior descending branch of the left coronary artery. Healthy and ischemic regions could clearly be distinguished by the differences in deformation.

Animals↗
PubMed1986

Gradients in fiber shortening and metabolism across ischemic left ventricular wall.

Blood flow, metabolism, and fiber shortening in various layers of left ventricular wall were studied during the initial 5 min of ischemia. In open-chest dogs (n = 51) ischemia was induced by coronary arterial stenosis (median value of mean perfusion pressure distal to stenosis 3.3 kPa). Epicardial deformation measurements with an inductive technique allowed estimation of fiber shortening in inner (eendo,est) and outer layers (eepi) of left ventricular free wall during the ejection phase. The decrease of eendo,est occurred within a few seconds after onset of stenosis, whereas eepi started to decrease 30 s later. After 1 min, eendo,est diminished to zero concomitantly with a reduction of blood flow and creatine phosphate content in the inner layers by 68 and 46%, respectively. In contrast a 60% reduction of eepi was associated with a decrease in blood flow of only 32% and no significant decrease in creatine phosphate in the outer layers. H+ and inorganic phosphate were released simultaneously into the local venous blood starting within 1 min of ischemia. During the initial 5 min of ischemia the content of ATP and glycogen remained unchanged across the ischemic wall. Present results indicate that the decrease of fiber shortening in the inner layers is associated with severe metabolic dearrangements, as reflected by the depletion of creatine phosphate. They also indicate that, during coronary arterial stenosis, impaired fiber shortening in the outer layers may result from the impairment of mechanical function in the inner layers, rather than from metabolic disturbances in the outer layers themselves.

Animals↗
PubMed1984

Fiber shortening in the inner layers of the left ventricular wall as assessed from epicardial deformation during normoxia and ischemia.

A mathematical model of left ventricular mechanics predicts that fiber shortening in the inner layers of the left ventricular wall can be estimated (eendo, est) from the magnitude of minimal (emin, o) and maximal shortening (emax, o) of the outer surface (= epicardium) of this wall. To evaluate this prediction, eendo, est and emin, o were compared with the shortening in the inner layers approximately along the fiber direction (eendo) as measured directly, before and during one minute of coronary artery occlusion. Deformation of the epicardium and the inner layers was determined by measuring mutual motion and angulation of three needles pierced into the myocardial wall, using an electromagnetic inductive technique. The proposed linear relations of eendo, est and emin, o with eendo were found to be significant. The needles hardly influenced wall deformation since similar values of epicardial deformation were found in separate, comparable, experiments (n = 13) using a triplet of epicardial coils. So eendo, est and emin, o are useful estimates of fiber shortening in the inner layers during normoxia and ischemia, especially when the time course of events is followed in the same animal.

Animals↗
PubMed1984

Accumulation of nonesterified fatty acids in ischemic canine myocardium.

In ischemic myocardium the time course of nonesterified fatty acid (NEFA) accumulation was studied in relation to changes in regional metabolism and mechanics. In open-chest dogs a coronary artery was partially occluded for 120 min. In the ischemic myocardium no increase was observed in NEFA content within 10 min, whereas changes were found in regional shortening, high-energy phosphate content, and glucose arteriologcal venous difference. During prolonged ischemia NEFA content increased, the highest values being found in the inner and middle layers after 120 min (112 and 85 nmol X g-1, respectively; control values 30); the value in the outer layers after 60 min was 93 nmol X g-1. After 120 min of ischemia, accumulation of NEFA generally occurred when myocardial blood flow was below 0.3 ml X min-1 X g-1 and ATP content was below 10 mumol X g dry wt-1. Under these circumstances the individual NEFA with the highest relative increase was arachidonic acid. The present findings indicate that the changes in mechanical function and metabolism, as observed in myocardium rendered ischemic for 10 min, are not caused by increased NEFA content and that NEFA accumulation may partly result from hydrolysis of glycerophospholipids.

Adenosine Triphosphate↗
PubMed1982

Uptake and tissue content of fatty acids in dog myocardium under normoxic and ischemic conditions.

The effect of ischemia on the myocardial content of nonesterified fatty acids (NEFA), triacylglycerol, cholesteryl esters, and phospholipids assayed with gas-liquid chromatography was studied in an open-chest dog preparation. Ischemia was induced by partial occlusion of the left interventricular coronary artery during 120 minutes (n = 20). Tissue content of the lipid classes was assessed in biopsies taken from ischemic and normoxic areas of the left ventricular free wall. Local venous blood from the concomitant vein of the left interventricular coronary artery was collected to determine myocardial extraction of lipids. In eight other dogs, no ischemia was induced (control group). Under normoxic conditions, NEFA appeared to be present in trace amounts: about 25 nmol/g wet weight of tissue, representing less than 0.1% of total myocardial fatty acids. During ischemia, NEFA increased in the affected area. This accumulation was most pronounced in the least perfused layer: the subendocardium (up to 172 nmol/g). Blood flow, estimated with radioactively labeled microspheres fell from 0.55 to 0.06 ml/min per g in this particular layer. The uptake of NEFA by the ischemic myocardium was decreased, indicating that enhanced lipolysis of endogenous lipids or reduced combustion may be held responsible for the accumulation of NEFA in ischemic tissue. Since arachidonic and linoleic acids showed the highest relative increase, lipolysis of endogenous phospholipids, rich in these fatty acids, seems to be reasonable. Ischemia had no significant effect on the content of triacylglycerol and cholesteryl esters. Phospholipids tended to decrease in the affected subendocardial layers.

Animals↗
PubMedDate not supplied

Coronary artery stenosis controlled by distal perfusion pressure: description of the servo-system and time-dependent changes in regional myocardial blood flow.

An animal model for the induction of coronary artery stenosis is described. In this model the degree of stenosis, as induced with commercially available hydraulic occluders, can be easily controlled by keeping constant the mean perfusion pressure (pcor) distal to the site of stenosis. This pcor is the input signal for a servo-system feeding a motor-pump, which determines the degree of inflation of the cuff around the left anterior interventricular coronary artery (LAICA). In each experiment pcor did not vary more than 2 mm Hg from the preset value of about 25 mm Hg. In 60 anesthetized open-chest dogs the time course of standard hemodynamic variables and regional myocardial blood flow in the center of the underperfused area, using the radioactive microsphere technique, were determined. Within 1 min after induction of stenosis heart rate and end-diastolic left ventricular pressure (plved) increased (by 20 and 60%, respectively) and mean aortic pressure and dplv/dtmax decreased (by 10 and 25%, respectively). After the initial decrease median myocardial blood flow further decreased between 1 and 5 min of stenosis from 0.63 to 0.32 ml.min-1.g-1 in the outer layers (P less than 0.05) and from 0.26 to 0.15 ml.min-1.g-1 in the inner layers (P less than 0.05), despite constant hemodynamic conditions and pcor. Between 5 and 120 min of stenosis these values remained unchanged in the outer layers, but decreased further in the inner layers to 0.08 ml.min-1.g-1 (P less than 0.05). The accurate control of pcor, the reproducibility of the levels of residual blood flow and the ease of handling the stenosis system indicate that coronary artery stenosis controlled by perfusion pressure distal to the stenosis is a useful animal model to study events during regional myocardial ischemia. With the use of this model of low flow ischemia a biphasic increase of myocardial vascular resistance was observed, which is initiated during the first minutes of coronary artery stenosis.

Animals↗
PubMedDate not supplied

The effect of elevated arterial free fatty acid concentrations on hemodynamics and myocardial metabolism and blood flow during ischemia.

In the present investigation the effect of elevated arterial free fatty acid (FFA) concentrations on regional myocardial blood flow (MBF), myocardial metabolism and hemodynamics during ischemia was studied in anesthetized dogs. Ischemia was induced by stenosis of the left interventricular coronary artery. Mean poststenotic coronary artery pressure was kept constant during ischemia. FFA concentrations were elevated by intravenous injection of heparin (group I), intralipid (group II) or both substances (group III). After elevation of FFA concentrations by heparin alone or together with intralipid, heart rate gradually increased, while aortic pressure tended to decrease. Slight elevation of arterial FFA levels (up to 0.30 mM, group I, and up to 0.53 mM, group II) had no significant effect on total MBF and uptake of glucose, FFA, and oxygen or release of lactate in the ischemic myocardium. However, elevating arterial FFA levels up to 0.81 mM (Group III), significantly decreased total MBF (6%), endo/epicardial blood flow ratio (13%), and oxygen uptake (34%) in the ischemic myocardium and resulted in release of lactate from this area. The release of potassium, inorganic phosphate and H+ as well as plasma CO2 concentration were not influenced. Neither was the uptake of glucose and FFA. These findings suggest that elevated arterial FFA concentrations can decrease MBF and augment lactate production in the ischemic myocardium.

Animals↗