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Biomedical subjects

R S Reneman

Publications and source records attributed to R S Reneman.

At least 181 records · Page 10Linked to original sources
PubMed1990

Noise reduction in estimating cardiac deformation from marker tracks.

Deformation of the cardiac wall is measured by using optical or radiopaque markers attached to the wall. When digitized images are used, the accuracy of the measurement of a marker position is limited by pixel resolution and the size of the marker. The spatial accuracy is improved by singular value decomposition (SVD) filtering. This filtering procedure is based on the assumption that displacements of markers are mutually related because they are embedded in a common continuum. In a computer stimulation with 48 markers in 51 video frames, the accuracy of the measurement of a marker position improved from 0.14 to 0.045 (SD) pixel. In an open-chest animal experiment, with markers on the surface of the heart, the deformation patterns were extracted more clearly using SVD filtering, while mutually related high-frequency components were not suppressed. In a 50-frame sequence of 256 X 256 video images of a 45 mm X 35 mm deforming surface with 50 markers of 8 pixels in diameter, the marker position resolution improves from 0.1 to 0.03 (SD) pixel (6 microns). Strain is determined with an accuracy of 0.002 over a distance of 30 pixels (6 mm).

Animals↗
PubMed1990

Ischemia and reperfusion induced formation of eicosanoids in isolated rat hearts.

Isolated, ejecting rat hearts, perfused with Krebs-Henseleit buffer, were exposed to various periods of global ischemia. Arachidonic acid (AA) accumulated significantly in the ischemic heart when the duration of ischemia exceeded 45 min. During 30 min of reperfusion, tissue levels of AA raised steadily to values of 10.5, 17.7, and 63.1 nmol/g, after 30, 45, and 60 min of ischemia, respectively. During reperfusion, significant amounts of AA metabolite prostacyclin (determined as stable metabolite 6-ketoprostaglandin F1 alpha, by radioimmunoassay and high-performance liquid chromatography) were released after 30, 45, and 60 min of ischemia. Beside prostacyclin, only small amounts of thromboxane B2 could be found during reperfusion. In contrast to increasing amounts of AA in reperfused tissue, prostacyclin release was maximal during the first 5 min of reperfusion and declined rapidly thereafter. Relatively small proportions of the accumulated AA are converted into prostacyclin, i.e., less than 1%. When hearts were treated with mepacrine, AA accumulation was almost completely abolished during 60 min of ischemia. The cumulative release of prostacyclin was found to be reduced to 134 pmol/g during 30 min of subsequent reperfusion. A close, rectilinear correlation could be established between AA accumulation and cumulative prostacyclin release during reperfusion. It is likely, however, that the site of bulk AA accumulation and that of conversion of AA into eicosanoids does not coincide in the ischemic and reperfused heart because of the low conversion rates of AA into prostacyclin and the different time courses of AA accumulation and prostacyclin production after reinstallation of flow.

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↗
PubMed1990

Exercise-induced swelling of rat soleus muscle: its relationship with intramuscular pressure.

Exercise-induced tissue swelling and its possible consequence for tissue pressure were studied in rat soleus muscle. Rats ran for 75 min on a belt with a 10 degree positive incline. Wet weights of cryofixed soleus muscles were increased at 3 (16%), 6 (28%), 9 (16%), and 24 (16%) h after running compared with those of nonexercised controls. The transient increase in muscle wet weight correlated in time with an increase in muscle volume. Muscle fiber swelling accounted for most of the muscle swelling in absolute terms because of the large proportion (approximately 90%) of the muscle volume composed of fibers, but swelling of the interstitium was about twofold larger than fiber swelling per unit area. Muscle fiber degeneration was most frequently found at the end of the observation period, i.e., 24 h after running. The muscle swelling was not associated with an increase in intramuscular pressure. During the postexercise measuring period (18 min to 24 h after exercise), intramuscular pressures of exercised rats (1.3 +/- 0.3 mm Hg) did not differ significantly from control values (1.0 +/- 0.2 mm Hg). These findings indicate that increased intramuscular pressure is not responsible for the muscle fiber degeneration found in rat soleus muscle 24 h after endurance running.

Animals↗
PubMed1990

Recombinant human erythropoietin and its effects on macro- and microcirculation during normovolemia. A physiological study of hemodynamics, fluid status and skin microcirculation.

In 9 chronic hemodialysis patients, treated with recombinant human erythropoietin (rHuEpo), longitudinal studies were performed to investigate possible changes in macro- and microcirculatory parameters during normovolemia, as assessed echographically by determining the inferior vena cava diameter and adjusting dialysis dry weight. Hematocrit increased from 19 +/- 4 to 33 +/- 5% (p less than 0.001). Systemic vascular resistance increased from 1,020 +/- 259 to 1,283 +/- 245 dyn/s/cm-5 (p less than 0.02), while mean arterial pressure remained unchanged. Cardiac index decreased (4.9 +/- 1.4 to 3.8 +/- 0.9 liters/min/m2; p less than 0.02), caused by a decrease in heart rate (87 +/- 21 to 75 +/- 16 beats/min; p less than 0.02) and stroke index (59.9 +/- 15.2 to 51.0 +/- 10.7 ml/m2; p less than 0.02). Red blood cell volume increased (468 +/- 105 to 858 +/- 203 ml/m2; p less than 0.001) and plasma volume decreased inversely ([125I]-albumin; 2,008 +/- 338 to 1,664 +/- 225 ml/m2; p less than 0.001), whereas total blood volume remained unaltered (2,476 +/- 397 to 2,518 +/- 352 ml/m2; n.s.). Total body weight increased (57.8 +/- 12 to 62.1 +/- 12 kg; p less than 0.02), indicative of an anabolic effect of rHuEpo therapy. Skin capillary circulation as measured by transcutaneous oxymetry at 37 degrees C skin temperature impaired, reflected by the increase of the time to peak after arterial occlusion (82 +/- 21 to 121 +/- 25 s; p less than 0.02). The reactive hyperemic response following the release of occlusion showed a significant increase at high hematocrit (10.7 +/- 4.2 to 16.6 +/- 5.3 mm Hg; p less than 0.02), whereas resting transcutaneous Po2 values showed a slight but not significant increase (2.3 +/- 1.3 to 4.7 +/- 3.3 mm Hg; n.s.). The high number of pathological capillaries in hemodialyzed patients might be an additional factor for the increase in systemic vascular resistance.

Adult↗
PubMed1990

Influence of fluid removal during haemodialysis on macro- and skin microcirculation. Haemodynamic pathophysiologic study of fluid removal during haemodialysis.

Changes of macro- and microcirculation during haemodialysis and fluid removal are probably dependent on ultimate fluid status and on the efficacy of various regulation mechanisms, especially the catecholamines. This was studied in 20 chronic dialysis patients. Pre- and postdialysis stroke volume, mean arterial pressure, heart rate and systemic vascular resistance were measured. Furthermore, microcirculation was studied by Laser Doppler flow and by intravital microscopy of finger nail fold, measuring red blood cell velocity and capillary density. Pre- and postdialysis noradrenaline and adrenaline were measured. Nine patients proved to be hypovolaemic after dialysis (group I) and 11 patients proved to be normovolaemic or less hypervolaemic (group II) according to vena cava inferior parameters. There was a significant decrease of mean arterial pressure and stroke volume in group I, and an increase of heart rate, whereas in group II there was only a decrease of mean arterial pressure. Systemic vascular resistance did not change in both groups. Noradrenaline decreased although not significantly in both groups, whereas in group I adrenaline increased significantly. There was a significant decrease of skin perfusion in group I, whereas in group II there was a significant increase. Capillary density increased significantly in group II after reaching normovolaemia. Underhydration was leading to a decrease of skin microcirculation on the basis of a decrease of stroke volume and an increase of adrenaline levels. In hypervolaemic patients, who were ultrafiltrated to normovolaemia, skin microcirculation improved on the basis of a decrease of arterial and venous pressure and consequently a decrease of the myogenic response as a local autoregulatory effect.

Adult↗
PubMed1990

Complete recovery in plasma of enzymes lost from the heart after permanent coronary artery occlusion in the dog.

Plasma activities of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) were measured after permanent coronary artery occlusion in the dog. Cumulative release of enzymes in plasma was calculated from these data by using a previously validated two-compartment model for circulating enzymes. Regional myocardial ischemia was measured by injection of radiolabeled microspheres. After 48 hours, the dogs were killed, and a detailed map of left ventricular enzyme activity was obtained from 108 tissue samples. Cumulative release into plasma of CK and HBD was 96 +/- 20% and 112 +/- 26%, respectively, of the total activities depleted from the heart (mean +/- SD, n = 11). The scatter in these values is inherent to the calculations, and it is concluded that both enzymes are recovered completely in plasma and, thus, can be used as quantitative markers of injury. Discrepancies between this result and earlier reports on the recovery of CK are only partly apparent and can be explained partly by underestimation of the elimination rate of CK from plasma, irregardless of tissue edema and incomplete extraction of enzyme activity from tissue.

Animals↗
PubMed1990

Time course of cellular enzyme release in dog heart injury.

The transport time of enzyme from heart to plasma was studied in two experimental models. First, the enzyme alanine aminotransferase was slowly infused into the left ventricular wall in open-chest dogs. The half-life for the washout of alanine aminotransferase activity into plasma was 20 +/- 4 minutes (mean +/- SEM, n = 8) and was not different in ischemic and normally perfused tissue. From measurements of arteriovenous differences in alanine aminotransferase activity and left ventricular blood flow, it was concluded that 77 +/- 14% of total enzyme washout from ischemic tissue occurred by direct entry into the bloodstream. The corresponding value for the vascular permeability-surface area product was 264 +/- 55 ml.kg-1.hr-1. For a second model, we studied myocardial enzyme release into plasma after abrupt heart injury induced by 10 minutes of calcium-free coronary perfusion followed by reintroduction of calcium (calcium-paradox mechanism). The half-life for the release into plasma was 1.9 +/- 0.2 hours (mean +/- SEM, n = 6) and was again not influenced by sustained ischemia. Slower washout, as observed for this second model, is consistent with increased interstitial protein space and corresponds to a permeability--surface area product between 135 and 285 ml.kg-1.hr-1. These results were used to calculate the time course of cellular enzyme leakage from the rate of enzyme release into plasma in various forms of heart injury. Significant shifts between the time curves of evolving cellular injury and enzyme release into plasma are observed after 2 hours of ischemia followed by coronary reperfusion, but not after permanent ischemia.

Alanine Transaminase↗
PubMed1990

Determination of tissue motion velocity by correlation interpolation of pulsed ultrasonic echo signals.

Correlation interpolation is introduced as a method to determine the displacement of moving biological tissue on the basis of a sequence of ultrasonic echo signals. The echo signal is sampled along the echo depth with approximately 4 samples per average high frequency period. Sampling in time occurs with the pulse repetition frequency. The necessary information is extracted from a crosscorrelation function between successive signals, which is modelled using four parameters. The parameters are estimated from five calculated correlation sums and the shift with maximum correlation is determined. In contrast to existing techniques, the performance of this method is determined mainly by the number of samples used, while the ratio of the number of samples in depth and time is irrelevant. Using 64 samples at a signal-to-noise power ratio of 10, the standard deviation of the error in the determination of the shift in depth is 0.08 sampling intervals. As in many other methods, the width of the aliasing interval equals the mean frequency period.

Echocardiography, Doppler↗
PubMed1990

A two-dimensional numerical analysis of unsteady flow in the carotid artery bifurcation. A comparison with three-dimensional in-vitro measurements and the influence of minor stenoses.

In the present study a two-dimensional finite element model for incompressible Newtonian flow is applicated to the modelling of carotid artery flow. In earlier studies, the numerical model was validated experimentally for several flow configurations. In general the pulsatile flow is characterized by reversed flow regions at the non-divider side walls of both the internal and external carotid arteries. The unsteadiness of the flow is associated with rather complex spatial and temporal velocity distributions and leads to temporal variations of the location and length of the reversed flow regions. As a consequence, pronounced spatial and temporal variations in the wall shear stresses are found. At the non-divider side walls, wall shear stresses are relatively low and exhibits an oscillatory behaviour in space and time. At the divider side walls, wall shear stresses are relatively high and approximately follow the flow rate distribution in time. The aim of this study is not only to present two-dimensional calculations but also to compare the calculated two-dimensional velocity profiles with those from three-dimensional experiments. It is observed that in the common carotid artery and in the proximal parts of the internal and external carotid arteries, the two-dimensional numerical model provides valuable information with respect to the three-dimensional configuration. In the more distal parts of especially the internal carotid artery, deviations are found between the two-dimensional numerical and three-dimensional experimental model. These deviations can mainly be attributed to the neglect of the secondary velocity distribution in the two-dimensional model. In the two-dimensional numerical model the influence of a minor stenosis in the internal carotid artery is hardly distinguishable from a minor geometrical variation without stenosis. Full three-dimensional analyses of the influence of minor stenoses are needed to prove numerically whether in-vivo measurements of the axial velocity distribution are useful in the detection of minor stenoses.

Arterial Occlusive Diseases↗
PubMed1990

Changes in myocardial high-energy phosphate stores and carbohydrate metabolism during intermittent aortic crossclamping in dogs on cardiopulmonary bypass at 34 degrees and 25 degrees C.

The effect of cooling to 25 degrees C on myocardial metabolism was studied during four periods of global ischemia (10 minutes each) followed by 15 minutes of reperfusion in dogs on cardiopulmonary bypass. Systemic and heart temperature at normothermia (group N, 34 degrees C; n = 15) was compared with general hypothermia (group H, 25 degrees C; n = 16). Before and at the end of each aortic crossclamp period in small myocardial biopsy specimens the adenosine triphosphate, creatine phosphate, inorganic phosphate, glycogen, and lactate content was analyzed. Also, lactate and inorganic phosphate were measured in the coronary effluents during the repetitive periods of reperfusion. Hemodynamic function was not different at 60 minutes after cardiopulmonary bypass compared with pre-cardiopulmonary bypass values, and was not different between the groups N and H. The tissue content of adenosine triphosphate and glycogen decreased progressively during the experimental period, resulting in slightly depressed values in both groups at the end of cardiopulmonary bypass. Pronounced effects of ischemia and reperfusion on tissue content of creatine phosphate, inorganic phosphate, and lactate were observed after each period of ischemia. The net decrease in tissue creatine phosphate content was not different between groups N and H (41 +/- 4 versus 38 +/- 4 mumol.gm-1 dry weight; mean +/- standard error of the mean) after 10 minutes of ischemia. However, during ischemia the net inorganic phosphate increase in myocardial tissue was significantly higher in group H (70 +/- 7 mumol.gm-1) than in group N (44 +/- 3 mumol.gm-1). These findings do not support the notion that myocardial protection is improved during hypothermia. Moreover, quantitatively the release of inorganic phosphate and lactate did not correlate with the amount accumulated in the myocardial tissue during the preceding periods of ischemia. The release appeared to be temperature dependent, that is, significantly reduced at 25 degrees C. The present data demonstrate why clinical outcome is satisfactory in both surgical procedures, when in general the periods of aortic crossclamping do not exceed 10 minutes each and the reperfusion periods in between the ischemic episodes last about 15 minutes. Besides, the findings indicate that hypothermia is not strictly necessary under these circumstances.

Adenosine Triphosphate↗
PubMed1990

Experimental and numerical analysis of carotid artery blood flow.

To obtain more insight into the complex blood flow patterns in the carotid artery bifurcation numerical analyses, limited to Newtonian incompressible flows in rigid-wall geometries, have been carried out combined with laser-Doppler velocity measurements. The steady and unsteady flow in two-dimensional models of a stenosis and of the carotid artery bifurcation were analysed. As a first step to a three-dimensional analysis, the steady flow development in a curved tube was investigated.

Blood Flow Velocity↗
PubMed1990

Foot salvage and improvement of microvascular blood flow as a result of epidural spinal cord electrical stimulation.

Epidural spinal cord electrical stimulation has been suggested as an alternative treatment in patients with limb-threatening ischemia in whom vascular reconstructive surgery is not possible anymore. We studied the effects of epidural spinal cord electrical stimulation on microcirculatory blood flow in 20 patients with ischemic rest pain and ulcers. Angiography showed occluded crural arteries technically unsuitable for reconstructive surgery. Intravital capillary microscopy was used to assess capillary density and diameter and red blood cell velocity before and after a 1-minute period of arterial occlusion. After epidural spinal cord electrical stimulation 18 patients claimed immediate pain relief, which was confirmed by intravital capillary microscopy. Capillary density increased from 10 to 19/mm2 (p less than 0.001), red blood cell velocity increased from 0.088 to 0.496 mm/sec (p less than 0.001), and peak red blood cell velocity after arterial occlusion increased from 0.092 to 0.548 mm/sec (p less than 0.001). Two patients had no immediate pain relief; they did not show improvement of microcirculatory perfusion, and amputation was necessary. During the follow-up period (3 months to 3 years, mean 27 months), six other patients had recurrent ischemic pain, and amputation was necessary. In 12 patients pain relief continued, and ischemic ulcers healed; capillary microscopy confirmed improved microcirculatory blood flow. Microcirculatory parameters were significantly higher in respondents than in nonrespondents (p less than 0.001). Life-table analysis revealed a cumulative foot salvage of 80% and 56% after 1 and 2 years, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Nebivolol is devoid of intrinsic sympathomimetic activity.

Nebivolol is a chemically novel, potent and selective beta 1-adrenoceptor-blocking agent that acutely lowers arterial blood pressure in hypertensive patients and rats without depressing, or even enhancing, left ventricular function. These properties could be compatible with a partial agonistic effect of beta-adrenoceptor-blocking agents. It was the aim of the present study to investigate whether nebivolol has intrinsic sympathomimetic properties. The study was performed on reserpinized dogs and spontaneously hypertensive rats, and on various isolated tissues from various species. Unlike pindolol and practolol, nebivolol did not exert a stimulating effect on the heart rate and left ventricular function in reserpinized animals and/or in isolated atria of reserpinized rats at doses that are clinically active. Nebivolol did not induce relaxation of isolated coronary arteries and saphenous veins at concentrations that block beta-adrenoceptors. These findings indicate that nebivolol is devoid of intrinsic sympathomimetic activity at clinically relevant doses.

Adrenergic beta-Antagonists↗
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

Changes in vasomotion pattern and local arteriolar resistance during stepwise pressure reduction.

Changes in vasomotion parameters and their consequences for local arteriolar resistance were studied in transverse arterioles and their first order side branches in the tenuissimus muscle of 10 young urethane anesthetized rabbits during stepwise reduction of arterial pressure, using intravital microscopy. To assess the influence of vasomotion on mean local arteriolar resistance, the effective vascular diameter, as a measure of mean flow carrying capacity, was calculated. The contribution of vasomotion to the mean local resistance is limited in transverse arterioles, but important in first order side branches, dominating the flow fluctuations in the downstream capillaries. During pressure reduction, an over-all increase in vasomotion cycle length and amplitude was found in both transverse arterioles and first order side branches, concomitant with an increase in effective arteriolar diameter and a decrease in local blood flow and reduced velocity, as a measure of wall shear rate. Flow autoregulation was observed in 70% of the arterioles. The changes in cycle length and amplitude showed only limited correlations with local blood flow, reduced velocity, arterial pressure and effective arteriolar diameter. This indicates that it is unlikely that only one of these variables is responsible for the changes in the vasomotion parameters.

Animals↗
PubMed1989

Recovery of hypertrophied rat hearts after global ischemia and reperfusion at different perfusion pressures.

The ability to resist transient ischemia was studied in isolated hearts of 18 months old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Both types of hearts showed optimal performance during the preischemic period when perfused at a diastolic perfusion pressure of 8.0 (WKY) and 13.3 (SHR) kPa. Hemodynamic recovery of WKY hearts during reperfusion at 8.0 kPa, following 45 min global ischemia, was satisfactory. coronary perfusion completely normalized, contractility (dPlv/dtmax) was slightly depressed and cardiac output returned, on the average, to 40% of the preischemic values. In contrast, hemodynamic function of SHR hearts reperfused at 13.3 kPa was greatly depressed, as evidenced by almost complete abolition of cardiac output, severe reduction of dPlv/dtmax and persistent underperfusion of the endocardial layers. In addition, the postischemic release of lactate dehydrogenase was retarded and enhanced. The release patterns of degradation products of adenine nucleotides showed a shift to the endstage products xanthine and uric acid. The enhanced vulnerability of the hypertrophied heart to ischemia was even more expressed when the SHR hearts were reperfused at 8.0 kPa. Postischemic function was characterized by electrical instability, loss of contractility and cardiac output, and noreflow in the endocardial layers. Persistent accumulation of lactate and degradation products of adenine nucleotides in the postischemic hearts are in line with the lack of reperfusion. The present results indicate that a detailed mechanistic explanation for the reduced ability to withstand ischemia of SHR cannot be based on differences in ATP content or an altered anaerobic glycolitic activity prior and during ischemia. It is suggested that a defect on the circulatory level, probably caused by enhanced reactivity of the coronary vessels towards ischemia-elicited factors, is responsible for the higher vulnerability of hypertrophied heart to an ischemia insult.

Adenosine Triphosphate↗