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Biomedical subjects

F W Prinzen

Publications and source records attributed to F W Prinzen.

At least 19 recordsLinked to original sources
PubMed2000

Blood flow distributions by microsphere deposition methods.

The art and science of the use of deposition markers for the estimation of blood flow distributions throughout the body and within organs is reviewed. Development of diffusible tracer techniques started 50 years ago. Twenty years later, radioactive 15 micron microspheres became the standard marker. Early studies on small animals, fetal sheep in 1967 and rats in 1976, provoked much of the technical development. Needs for avoiding the use of radioactivity, for having long lasting labels, and for providing higher spatial resolution, are driving the continuing exploration of newer techniques using colored and fluorescent microspheres and molecular deposition markers. Strengths and weaknesses of the various methods are compared.

Animals↗
PubMed1999

Hyperoxia and local organ blood flow in the developing chick embryo.

1. Hyperoxia can cause local vasoconstriction in adult animal organs as a protective mechanism against hyperoxia-induced toxicity. It is not known at what time during development this vasoconstrictor capacity is present. Therefore, we measured the cardiac output (CO) distribution in different organs during a period of acute hyperoxia (100 % O2) in the developing chick embryo. 2. Fertile eggs were divided into five incubation time groups (10 and 11, 12 and 13, 14 and 15, 16 and 17, and 18 and 19 days of a normal incubation time of 21 days). Eggs were opened at the air cell and a catheter was inserted into a branch of the chorioallantoic vein for injections of 15 microm fluorescent microspheres during normoxia and at the end of 5 min (test group 1; n = 39) or 20 min (test group 2; n = 21) of hyperoxia exposure (100 % O2). The fraction of CO to an organ was calculated as the fluorescence of the organ sample divided by the sum of the fluorescence of all organs. 3. Only in 18- and 19-day-old embryos did hyperoxia cause a decrease in the fractions of CO to the heart and carcass, and an increase in those to the yolk-sac and chorioallantoic membrane. This response was more pronounced after 20 min (test group 2) than after 5 min (test group 1) of hyperoxia with an additional decrease in the fractions of CO to the brain, intestine and liver (test group 2). 4. These data indicate that local mechanisms for hyperoxia-induced vasoconstriction in the heart, brain, liver, intestine and carcass develop late, during the final 15 % of the incubation period, in the developing chick embryo.

Animals↗
PubMed1999

Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging.

OBJECTIVES: The purpose of this study was to determine the spatial distribution of myocardial function (myofiber shortening and work) within the left ventricular (LV) wall during ventricular pacing. BACKGROUND: Asynchronous electrical activation, as induced by ventricular pacing, causes various abnormalities in LV function, perfusion and structure. These derangements may be caused by abnormalities in regional contraction patterns. However, insight into these patterns during pacing is as yet limited. METHODS: In seven anesthetized dogs, high spatial and temporal resolution magnetic resonance-tagged images were acquired in three orthogonal planes. Three-dimensional deformation data and LV cavity pressure and volume were used to determine midwall circumferential strain and external and total mechanical work at 192 sites around the left ventricle. RESULTS: During ventricular pacing, systolic fiber strain and external work were approximately zero in regions near the pacing site, and gradually increased to more than twice the normal value in the most remote regions. Total mechanical work, normalized to the value during right atrial pacing, was 38 +/- 13% (right ventricular apex [RVapex] pacing) and 61 +/- 23% (left ventricular base [LVbase] pacing) close to the pacing site, and 125 +/- 48% and 171 +/- 60% in remote regions, respectively (p < 0.05 between RVapex and LVbase pacing). The number of regions with reduced work was significantly larger during RVapex than during LVbase pacing. This was associated with a reduction of global LV pump function during RVapex pacing. CONCLUSIONS: Ventricular pacing causes a threefold difference in myofiber work within the LV wall. This difference appears large enough to regard local myocardial function as an important determinant for abnormalities in perfusion, metabolism, structure and pump function during asynchronous electrical activation. Pacing at sites that cause more synchronous activation may limit the occurrence of such derangements.

Animals↗
PubMed1999

Kinematic analysis of left ventricular deformation in myocardial infarction using magnetic resonance cardiac tagging.

The Magnetic Resonance (MR) tagging technique provides detailed information about 2D motion in the plane of observation. Interpretation of this information as a reflection of the 3D motion of the entire cardiac wall is a major problem. In finite element models of the mechanics of the infarcted heart, an infarcted region causes motional asymmetry, extending far beyond the infarct boundary. Here we present a method to quantify such asymmetry in amplitude and orientation. For this purpose images of a short-axis cross-section of the ejecting left ventricle were acquired from 9 healthy volunteers and 5 patients with myocardial infarction. MR-tags were applied in a 5 mm grid at end-diastole. The tags were tracked by video-image analysis. Tag motion was fitted to a kinematic model of cardiac motion. For the volunteers and the patients the center of the cavity displaced by about the same amount (p = 0.11) during the ejection phase: 3.8 +/- 1.4 and 3.0 +/- 0.9 mm (mean +/- sd), respectively. Cross-sectional rotation and the decrease in cross-sectional area of the cavity were both greater in the volunteers than in the patients: 6.4 +/- 1.5 vs. 3.0 +/- 0.8 degrees (p < 0.001), and 945 +/- 71 vs. 700 +/- 176 mm2 (p = 0.02), respectively. In the patients, asymmetry of wall motion, as expressed by a sine wave dependency of contraction around the circumference, was significantly enlarged (p = 0.02). The proposed method of kinematic analysis can be used to assess cardiac deformation in humans. We expect that by analyzing images of more cross-sections simultaneously, the 3D location and the degree of infarction can be assessed efficiently.

Biomechanical Phenomena↗
PubMed1999

Mapping propagation of mechanical activation in the paced heart with MRI tagging.

The temporal evolution of three-dimensional (3-D) strain maps derived from magnetic resonance imaging (MRI) tagging were used to noninvasively evaluate mechanical activation in the left ventricle (LV) while seven canine hearts were paced in situ from three different sites: the base of the LV free wall (LVb), the right ventricular apex (RVa), and the right atrium (RA). Strain maps plotted against time showed the evolution of shortening over the entire LV midwall and were used to generate mechanical activation maps showing the onset of circumferential shortening. RA pacing showed rapid synchronous shortening; LVb pacing showed a wave front of mechanical activation propagating slowly and steadily from the pacing site, whereas RVa pacing showed regions of rapid and slower propagation. The mechanical (M) activation times correlated linearly with the electrical (E) activation (M = 1.06E + 8.4 ms, R = 0.95). The time for 90% activation of the LV was 63.1 +/- 24.3 ms for RA pacing, 130.2 +/- 9.8 ms for LVb pacing, and 121.3 +/- 17.9 ms for RVa pacing. The velocity of mechanical activation was calculated for LVb and RVa pacing and was similar to values reported for electrical conduction in myocardium. The propagation of mechanical activation for RVa pacing showed regional variations, whereas LVb pacing did not.

Animals↗
PubMed1998

Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall.

BACKGROUND: Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. METHODS AND RESULTS: Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2+/-10.6 to 113+/-16.5 ms acutely and to 133.8+/-25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27+/-15% and 15+/-17%, respectively. The early-activated LV free wall became significantly (17+/-17%) thinner, whereas the late-activated septum thickened significantly (23+/-12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39+/-13%. In paced animals, cardiomyocyte diameter was significantly (18+/-7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. CONCLUSIONS: Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.

Animals↗
PubMed1998

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time.

1. The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. 2. Fertilized eggs were studied at three incubation times (10-13 days, 14-16 days and 17-19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 micron fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. 3. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (-3 to -65 % of baseline), yolk-sac (-46 to -77 % of baseline) and carcass (-6 to -33 % of baseline). 4. The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. 5. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

Animals↗
PubMed1998

Imaging asynchronous mechanical activation of the paced heart with tagged MRI.

A method for imaging the rapid temporal-spatial evolution of myocardial deformations in the paced heart is proposed. High time resolution-tagged MR images were obtained after stimulation of the myocardium with an MR-compatible pacing system. The images were analyzed to reconstruct dynamic models of local 3D strains over the entire left ventricle during systole. Normal canine hearts were studied in vivo with pacing sites on the right atrium, left ventricular free wall and right ventricular apex. This method clearly resolved local variations in myocardial contraction patterns caused by ventricular pacing. Potential applications are noninvasive determination of electrical conduction abnormalities and the evaluation of new pacing therapies.

Animals↗
PubMed1998

Estimates of regional work in the canine left ventricle.

Assessment of the magnitude of regional myocardial work requires knowledge of regional fiber stress and fiber shortening. The theoretical development and experimental validation of a method is presented which used values of estimated active and passive fiber stress according to a fluid-fiber model, and measured fiber strain values. This enables the construction of regional stress-strain diagrams, a regional analog of the pressure-volume area model by Suga and co-investigators, which can be linked to regional oxygen consumption. In the left ventricle, either normally or asynchronously activated, the method yields reliable data on strain and active and passive fiber stress. The relation between estimated regional work and myocardial oxygen demand is in quantitative agreement with previously reported relations between global oxygen demand and measured pressure-volume area. During coronary artery occlusion, however, these values were less reliable, which might be due to inaqdequate knowledge of the (passive) material properties of the myocardium.

Animals↗
PubMed1998

Optimization of ventricular function by improving the activation sequence during ventricular pacing.

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowprobe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 +/- 5 ms during sinus rhythm and increased to 110 +/- 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8% +/- 7% and 15% +/- 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex (15% +/- 16%, 10% +/- 12% [P < 0.05], and 15% +/- 10%, respectively) and LV base pacing (11% +/- 12% [P < 0.05], 3% +/- 12%, and 3% +/- 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.

Animals↗
PubMed1998

Fluorescent microspheres are superior to radioactive microspheres in chronic blood flow measurements.

The accuracy of the fluorescent (FM) and radioactive microsphere (RM) techniques is similar in acute experiments but has not been established in chronic experiments. In the present study various combinations (at least pairs) of FM and/or RM labels were injected simultaneously between 2 mo and 5 min before each animal was killed. Blood flow was determined in many organs. Intramethod mean difference and variation did not change over time for FM but increased significantly for RM (from 1.8 +/- 1.4 to 25.6 +/- 21.8% and from 4.4 +/- 3.2 to 32.4 +/- 23.0% at 5 min and 2 mo, respectively). Also the FM-RM intermethod mean difference and variation increased (from -0.5 +/- 8.5 to 40.8 +/- 23.8% and from 23. 6 +/- 4.6 to 71.8 +/- 34.3%, respectively). After 2 mo, blood flow estimations were 20-50% lower with the various RM, whereas brain and liver blood flow values varied even more between isotopes. Underestimation started within 1 day for 51Cr and within 2 wk for 141Ce, 95Nb, and 85Sr. We conclude that FM are superior to RM for blood flow determination in experiments lasting longer than 1 day, presumably because of leaching of isotopes from RM.

Animals↗
PubMed1997

Cardiac output distribution in the chick embryo from stage 36 to 45.

OBJECTIVE: The distribution of cardiac output to different organs is well described in the mammalian fetus. Chick embryos are not often used in perinatal cardiovascular research and therefore it is not known whether they can serve as an animal model for this purpose. In this study we documented cardiac output distribution in chick embryos at increasing incubation time. METHODS: Fertilized eggs from day 10 to 19 with an incubation time of 21 days were studied in 3 increasing incubation time groups (10-13, 14-16 and 17-19 days). For the experiment, the egg was placed in a holder in an incubator. The egg was opened at the air cell and a small vein of the chorioallantoic membrane was catheterized. Twenty thousand fluorescent 15 microns microspheres in 0.2 ml were injected. After 5 min, the embryo was sacrificed and the different organs were dissected and digested for microsphere isolation and subsequent fluorescence analysis. RESULTS: The chorioallantoic membrane, which is the placenta equivalent of the chick embryo, received a relatively large fraction of the combined cardiac output: 52.08% (interquartile range [IQR] 12.67%) on days 10-13 and 40.95% (IQR 27.24%) on days 17-19. Relatively small fractions were distributed: to the heart 2.03% (IQR 1.58) on days 10-13 and 3.18% (IQR 1.95) on days 17-19, and to the brain 3.20% (IQR 1.80) on days 10-13 and 5.02% (IQR 3.39) on days 17-19. As incubation time advanced, the fraction of the combined cardiac output to the chorioallantoic membrane and yolk-sac decreased significantly in favor of the heart and brain. CONCLUSION: This distribution shows great similarity to the one found in the mammalian fetus. The chick embryo is an attractive model for perinatal cardiovascular research.

Allantois↗
PubMed1997

Relation between torsion and cross-sectional area change in the human left ventricle.

During the ejection phase, motion of the left ventricular (LV) wall is such that all myocardial fibers shorten to the same extent. In a mathematical model of LV mechanisms it was found that this condition could be satisfied only if torsion around the long axis followed a unique function of the ratio of cavity volume to wall volume. When fiber shortening becomes non-uniform due to cardiac pathology, this pathology may be reflected in aberration of the torsional motion pattern. In the present study we investigated whether the predicted regular motion pattern could be found in nine healthy volunteers, using Magnetic Resonance Tagging. In two parallel short-axis cross-sections, displacement, rotation, and area ejection were derived from the motion of tags, attached non-invasively to the myocardium. Information from both sections was combined to determine area ejection, quantified as the change in the logarithm of the ratio of cavity area to wall area, and torsion, represented by the shear angle on the epicardium. Linear regression was applied to torsion as a function of area ejection. The slope thus found (-0.173 +/- 0.024 rad, mean +/- S.D.) was similar to the slope as predicted by the model of LV mechanics (-0.194 +/- 0.026 rad). In conclusion, the relation between area ejection and torsion could be assessed noninvasively in humans. In healthy volunteers, the relation was close to what was predicted by a mathematical model of LV mechanics, and also close to what was found earlier in experiments on animals.

Algorithms↗
PubMed1997

Alleviation of the peripheral hemodynamic effects of dexmedetomidine by the calcium channel blocker isradipine.

BACKGROUND: Alpha 2-adrenergic agonists have peripheral vasoconstrictive effects and central sympatholytic and sedative effects. Whereas the latter are the basis of their use in anesthesia, the former could limit their clinical application. METHODS: To study whether a vasodilator could alleviate the systemic and coronary vasoconstrictor effects of dexmedetomidine without influencing the central sympatholytic effects, the calcium channel blocker isradipine was infused after a high dose of dexmedetomidine in anesthetized dogs. RESULTS: Dexmedetomidine 10 micrograms.kg-1 decreased plasma concentrations of norepinephrine and epinephrine by more than 90%, heart rate by 39%, cardiac output by 64%, dp/dtmax by 29% and increased mean arterial pressure by 55% and the left ventricular end-diastolic pressure (LVEDP) 4-fold as compared to baseline. In addition, coronary blood flow decreased by 52% and coronary venous oxygen saturation by 51%. Isradipine could completely antagonize all the coronary and systemic hemodynamic changes induced by dexmedetomidine, but only partially he increase in LVEDP. Isradipine caused no changes in plasma catecholamine levels. CONCLUSION: Isradipine could alleviate the peripheral hemodynamic actions of dexmedetomidine while having no effect on its central sympatholytic properties.

Adrenergic alpha-Agonists↗
PubMed1997

Hemodynamic and coronary vascular effects of dexmedetomidine in the anesthetized goat.

BACKGROUND: In phase III trials, the hemodynamic stabilising effect of the alpha 2-adrenergic agonist dexmedetomidine (DEX) is being investigated in patients with coronary artery disease, Coronary vascular effects of alpha 2-agonists have been studied in dogs and pigs, but both species have a different hemodynamic response to DEX than man. The aim of this study was to investigate the hemodynamic and coronary vascular effects in goats. METHODS: In 6 open-chest goats anesthetized with halothane, central and coronary hemodynamics and oxygen supply and demand were measured before and following IV bolus infusion of DEX in doses ranging from 0.1 to 10 micrograms/kg. RESULTS: With DEX doses of 1 microgram/kg or higher, mean arterial pressure (MAP), systemic vascular resistance, coronary vascular resistance and arterio-mixed venous oxygen content increased within 2 min, but returned to baseline within 15 min. In contrast, there was a progressive and cumulative decrease in cardiac output (CO), heart rate, and dP/dtmax, Regional coronary venous oxygen extraction (C(a-cv)O2) transiently increased after 3 micrograms/kg DEX and decreased 15 min after 10 micrograms/kg DEX. LVEDP transiently increased after 3 and 10 micrograms/kg DEX. The changes after DEX 10 micrograms/kg differed from those after lower doses: MAP (35%), CO (50%), stroke volume (33%), C(a-cv)O2 (15%) and myocardial oxygen extraction (33%) were all decreased. Myocardial oxygen supply and demand decreased in parallel. CONCLUSIONS: 1) The cardiovascular response to IV DEX in goats is similar to man. 2) In goats after DEX, systemic and coronary vasoconstriction are short-lived, and 3) the balance between myocardial oxygen supply and demand is maintained.

Adrenergic alpha-Agonists↗
PubMed1996

Coronary vascular effects of dexmedetomidine during reactive hyperemia in the anesthetized dog.

OBJECTIVE: The central sympatholytic effects of alpha2-adrenergic agonists are believed to be beneficial during myocardial ischemia, but the peripheral vasoconstrictive effects are controversial. The aim of this study was to investigate the coronary vascular effects of dexmedetomidine (DM) during reactive hyperemia. DESIGN: The study had a prospective, randomized, open-comparative design. SETTING: University animal laboratory. PARTICIPANTS: Nine mongrel dogs. INTERVENTIONS: Coronary artery occlusions lasting 2 minutes were induced five times at 40-minute intervals. DM, 0.1, 1, and 10 micrograms/kg was administered 15 minutes before the second, third, and fourth coronary occlusion, respectively. The alpha2-antagonist atipamezole was administered before the fifth coronary occlusion. MEASUREMENTS AND MAIN RESULTS: DM, 1 microgram/kg, significantly decreased heart rate (from 128 +/- 13 to 96 +/- 21 beats/min); 10 micrograms/kg of DM also significantly decreased cardiac output (from 3.4 +/- 1.1 to 1.4 +/- 0.4 L/min). DM decreased myocardial blood flow in all layers of normally perfused myocardium. In hyperemic myocardium, DM significantly decreased epicardial blood flow (from 3.30 +/- 1.43 to 1.44 +/- 0.49 mL/min/g after DM 10 micrograms/kg), whereas endocardial blood flow did not change, hereby significantly increasing the endo/epi blood flow ratio (from 0.99 +/- 0.54 to 2.28 +/- 0.78). CONCLUSIONS: In the postischemic hyperemic subendocardial layer, coronary blood flow was preserved after DM. DM reduced primary determinants of myocardial oxygen demand. These effects of DM may be beneficial in conditions of temporary coronary artery occlusion and subsequent reperfusion.

Adrenergic alpha-Agonists↗
PubMed1996

Beneficial effects of dexmedetomidine on ischaemic myocardium of anaesthetized dogs.

We have studied the effect of dexmedetomidine during coronary artery stenosis (CAS) in dogs. Three periods of 15 min of CAS were induced at 40-min intervals in two groups of dogs (dexmedetomidine compared with placebo). Dexmedetomidine was administered before the second and third periods of CAS in doses of 1 and 3 micrograms kg-1, respectively. Dexmedetomidine decreased plasma concentrations of noradrenaline by mean 71 (SEM 9)%, heart rate by 8 (4)%, cardiac output by 30 (6)% and increased mean arterial pressure by 23 (10)%. Dexmedetomidine reduced blood flow in non-ischaemic myocardium and in the ischaemic epicardial layer by 16 (8)%, but blood flow was preserved in the ischaemic mid-myocardial and subendocardial layers. Consequently, dexmedetomidine increased the ischaemic-non-ischaemic blood flow ratio. Dexmedetomidine did not change myocardial oxygen consumption but decreased myocardial oxygen demand from 4.91 (0.33) to 3.76 (0.25) mumol min-1 g-1, thereby reducing the oxygen deficiency of the ischaemic myocardium from 1.47 (0.37) to 0.29 (0.32) mumol min-1 g-1.

Adrenergic alpha-Agonists↗