Biomedical subjects

R S Reneman

Publications and source records attributed to R S Reneman.

At least 109 records · Page 6Linked to original sources

PubMed1994

Influence of endocardial-epicardial crossover of muscle fibers on left ventricular wall mechanics.

The influence of variations of fiber direction on the distribution of stress and strain in the left ventricular wall was investigated using a finite element model to simulate the mechanics of the left ventricle. The commonly modelled helix fiber angle was defined as the angle between the local circumferential direction and the projection of the fiber path on the plane perpendicular to the local radial direction. In the present study, an additional angle, the transverse fiber angle, was used to model the continuous course of the muscle fibers between the inner and the outer layers of the ventricular wall. This angle was defined as the angle between the circumferential direction and the projection of the fiber path on the plane perpendicular to the local longitudinal direction. First, a reference simulation of left ventricular mechanics during a cardiac cycle was performed, in which the transverse angle was set to zero. Next, we performed two simulations in which the spatial distribution of either the transverse or the helix angle was varied with respect to the reference situation, the spatially averaged variations being about 3 and 14 degrees, respectively. The changes in fiber orientation hardly affected the pressure-volume relation of the ventricle, but significantly affected the spatial distribution of active muscle fiber stress (up to 50% change) and sarcomere length (up to 0.1 micron change). In the basal and apical region of the wall, shear deformation in the circumferential-radial plane was significantly reduced by introduction of a nonzero transverse angle. Thus, the loading of the passive tissue may be reduced by the endocardial-epicardial crossover of the muscle fibers.

Aorta↗

PubMed1994

Effect of sample window length on the correlation between RF signal and pulsed Doppler signal intensity.

Ultrasound pulsed Doppler systems, as used in medical applications, are based on the detection of the phase difference between a reference signal and the received radio frequency (RF) signal averaged over the sample window. Thereby, it is implicitly assumed that the phase of the received signal will increase linearly with depth. However, the ultrasound signal originates from particles with a random spatial distribution. Therefore, it may be anticipated that the accuracy of the estimate for the phase difference will not improve by elongating the sample window. To test this hypothesis, simulated random phase RF signals with various bandwidths were subjected to demodulation using a rectangular observation window of different lengths. It is concluded that the correlation coefficient between RF intensity and Doppler intensity goes down for long sample windows. Moreover, the coefficient of variation of the estimate for the intensity of the received signal decreases for an increasing length of the observation window. The variation coefficient of the Doppler amplitude remains very close to one for all signal and processing conditions. These observations demonstrate that for Doppler signal amplitude assessment, the effect of the length of the observation window should be taken into account.

Normal Distribution↗

PubMed1994

Subsample volume processing of Doppler ultrasound signals.

Processing of Doppler signals produced by pulsed Doppler systems is based on the assumption that the phase of the received high frequency ultrasound signals changes linearly with depth. However, the random spatial distribution of scatterers is not in accordance with this basic assumption. Consequently, averaging of the demodulated signal over an observation window, covering a few periods of the received signal, does not improve the estimate for the instantaneous quadrature components of the Doppler signal originating from a given depth. Hence, the accuracy of the Doppler velocity estimate is independent of the length of the observation window employed. However, splitting the observation window in subsample volumes, each with a length of one period at the emission frequency, and combining the Doppler signals of the subsample volumes at the last stage of signal processing, i.e., mean Doppler frequency estimation using the autocorrelation technique, results in a considerable reduction of the variance of the velocity estimate. Using a computer simulation of the signal processing involved, it is demonstrated that with subsample volume processing the variance of the velocity estimate attains the same variance as is expected for the RF cross correlation technique.

Signal Processing, Computer-Assisted↗

PubMed1994

The role of serotonin blockers in cardiac anesthesia.

In the complex setting of cardiac surgery and cardiopulmonary bypass, several potent mediators are released that by interacting may cause clinical syndromes like coronary ischemia, systemic hypertension, pulmonary hypertension, and renal failure. One of the mediators is serotonin, released from aggregating platelets, and causing vasoconstriction by activating S2-serotonergic receptors, particularly in patients with an impaired endothelial function, as in atherosclerosis. The most important available specific S2-serotonergic receptor antagonist is ketanserin. If administered during or after cardiac surgery, ketanserin lowers systemic and pulmonary blood pressure, and improves peripheral and pulmonary perfusion without causing reflex tachycardia or an increase in pulmonary shunt fraction.

Anesthesia↗

PubMed1994

Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.

In the cardiac left ventricle during systole mechanical load of the myocardial fibers is distributed uniformly. A mechanism is proposed by which control of mechanical load is distributed over many individual control units acting in the environment of the cell. The mechanics of the equatorial region of the left ventricle was modeled by a thick-walled cylinder composed of 6-1500 shells of myocardial fiber material. In each shell a separate control unit was simulated. The direction of the cells was varied so that systolic fiber shortening approached a given optimum of 15%. End-diastolic sarcomere length was maintained at 2.1 microns. Regional early-systolic stretch and global contractility stimulated growth of cellular mass. If systolic shortening was more than normal the passive extracellular matrix stretched. The design of the load-controlling mechanism was derived from biological experiments showing that cellular processes are sensitive to mechanical deformation. After simulating a few hundred adaptation cycles, the macroscopic anatomical arrangement of helical pathways of the myocardial fibers formed automatically. If pump load of the ventricle was changed, wall thickness and cavity volume adapted physiologically. We propose that the cardiac anatomy may be defined and maintained by a multitude of control units for mechanical load, each acting in the cellular environment. Interestingly, feedback through fiber stress is not a compelling condition for such control.

Adaptation, Physiological↗

PubMed1994

Reflex sympathetic dystrophy: result of autonomic denervation?

1. To investigate the nature of sympathetic dysfunction in the pathogenesis of reflex sympathetic dystrophy, the microcirculatory vasoconstrictive responses to dependency were investigated in the skin of the hand of 76 reflex sympathetic dystrophy patients with unilateral disease by means of laser Doppler flowmetry (in perfusion units) and capillary microscopy. The patients were divided into three stages according to their perception of skin temperature (stage I in the case of a stationary warmth sensation, stage II in the case of an intermittent warmth and cold sensation, and stage III in the case of a stationary cold sensation). The vasoconstrictive responses were induced by lowering of the affected hand. 2. As compared to controls, the mainly sympathetically mediated vasoconstrictive response at thermoregulatory level of the skin microcirculation, as measured by laser Doppler flowmetry, was attenuated at stage I (1.82 versus 1.41, P < 0.05), stage II (1.82 versus 1.09, P < 0.0001) and stage III (1.82 versus 1.14, P < 0.01), suggesting the involvement of sympathetic denervation at all stages of the reflex sympathetic dystrophy syndrome. This sympathetic denervation may also account for the observed increase in thermoregulatory skin blood flow at stage I as compared to controls (152 versus 81, P < 0.01). 3. Since sympathetic denervation has been reported to cause increased sensitivity of vascular structures to catecholamines, the decrease in thermoregulatory skin blood flow at stages II (54 versus 81, P < 0.05) and III (31 versus 81, P < 0.05), both as compared to controls, may result from hypersensitivity to catecholamines of skin microvessels. 4. The sympathetically independent vasoconstrictive response at the nutritive level of skin microcirculation, as measured by capillary microscopy, was impaired only at stage III as compared to controls (1.04 versus 2.06, P < 0.05). This divergence in microvascular reactivity upon dependency of the nutritive and thermoregulatory subsystems also supports the hypothesis of sympathetic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Evaluation of reproducibility of a vessel wall movement detector system for assessment of large artery properties.

OBJECTIVE: Arterial distensibility (DC) and compliance (CC) are vessel wall properties of large arteries that can be measured non-invasively with a custom made vessel wall movement detector system (VWMDS). This study investigated the reproducibility of this device in 10 volunteers. METHODS: To investigate intraobserver intrasession and intraobserver intersession variability, arterial diameter (D) and relative change in diameter during the heart cycle (delta D/D) were measured in the elastic common carotid artery, and in the muscular femoral and brachial arteries. Interobserver intrasession variability was examined in common carotid artery by two observers, while interobserver variability on the same image was assessed for common carotid and femoral arteries. Variability was expressed as the coefficient of variation. RESULTS: For common carotid artery, intraobserver intrasession variability was 7.9(SEM 1.6)% (delta D/D), 4.5(1.1)% (D), 8.3(1.3)% (DC), and 9.1(2.6)% (CC), respectively. In femoral artery it was 12.4(2.2)% (delta D/D), 2.7(0.6)% (DC), 13.4(2.2)% (DC), and 12.5(2.1)% (CC). For brachial artery it was 13.4(2.8)% (delta D/D), 2.5(0.5)% (D), 16.1(2.5)% (DC), and 15.6(2.6)% (CC). Intraobserver intersession variability was comparable to intraobserver intrasession variability for all vessels. Interobserver intrasession variability for common carotid artery was 11.3(2.6)% (delta D/D) and 8.6(1.9)% (D), but was larger for DC and CC. Interobserver variability on the same image was < 5% for common carotid and femoral arteries. CONCLUSIONS: In conclusion, the vessel wall movement detector system has a good technical reproducibility. Intraobserver intrasession and intersession variability are comparable, and are larger in muscular arteries. This might be due to a larger variation in tone of these arteries, which are under permanent neurohumoral control. Interobserver intrasession variability was larger than intraobserver variability and might be influenced by differences in observers' skill and spontaneous variation in vessel wall properties.

Adolescent↗

PubMed1994

Spontaneous leukocyte rolling in venules in untraumatized skin of conscious and anesthetized animals.

Intravital bright-field videomicroscopy was used to investigate whether leukocyte rolling can be observed under normal physiological conditions. We studied skin venules in trained conscious rats and anesthetized rats and mice without touching the skin itself. Leukocyte rolling was spontaneously present in all hindpaw venules of Lewis rats (diam 8-27 microns) and also in all mouse ear venules (Swiss, 13-38 microns; BALB/c, 12-56 microns). Rolling levels (in leukocytes/min, median and range) were 8 (3-15) in conscious rats, 9 (3-19) in anesthetized rats, 30 (5-160) in anesthetized Swiss mice, and 10 (3-22) in anesthetized BALB/c mice. These levels appeared to be independent of time. Noninvasive mechanical stimulation induced an average increase of 32%. Fluorescent labeling of leukocytes in vivo with acridine orange had no influence. In Swiss mice, the rolling velocity was < 50 microns/s for > 75% of the leukocytes (median 31 microns/s); this parameter did not correlate with reduced velocity (17-68 s-1) and hence wall shear rate. Our finding that leukocyte rolling is spontaneously present in skin venules of anesthetized and conscious animals suggests a constant vigilance of the host defense mechanisms in the skin.

Acridine Orange↗

PubMed1994

Heat shock improves ischemic tolerance of hypertrophied rat hearts.

The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoBHS and ShamHS, respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoBC) and nonheated (control) nonhypertrophied (ShamC) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoBHS and ShamHS hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoBHS hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoBHS hearts but was significantly increased in ShamHS hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.

Animals↗

PubMed1993

Different roles of prostaglandins in thromboembolic processes in arterioles and venules in vivo.

The involvement of prostaglandins in thromboembolic processes, as induced by wall puncture, was studied in rabbit mesenteric arterioles and venules using intravital videomicroscopy. Inhibition of prostaglandin formation with aspirin (100 mg/kg, i.v.) significantly increased in arterioles duration of embolization (from 91 to 200 s) and number of emboli produced (from 4 to 8.5 per vessel), while rate of embolus production was not influenced. In venules, aspirin only influenced embolization rate (a significant decrease from one embolus/14 s to one/23 s). Specific blockade of TXA2-receptors by sulotroban (30 mg/kg, i.v.) only influenced the arteriolar reaction: it significantly decreased embolization duration (from 560 to 218 s) and number of emboli produced (from 23 to 10 emboli per vessel), without affecting embolization rate. These findings indicate that both platelet activating and inhibiting prostaglandins play a more important role in thromboembolism in arterioles than in venules; this suggests a difference in prostaglandin synthetic capacity between arteriolar and venular endothelium.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1993

Asymmetrical changes in ventricular wall mass by asynchronous electrical activation of the heart.

Ventricular pacing causes asynchronous electrical activation of the ventricular wall, because impulse conduction occurs via muscle fibers rather than via the Purkinje system. Chronic (up to 3 months) ventricular pacing caused about 30% decrease of wall mass in early activated regions but did not change wall mass in late activated regions. These are the first data indicating that chronic asynchronous activation induces asymmetrical structural adaptations. This asymmetry is likely to be evoked by regional differences in contractile work, as demonstrated in previous experiments from our laboratory. The nature of the structural adaptation as well as its clinical implications deserve more detailed investigation.

Adaptation, Physiological↗

PubMed1993

Macroscopic three-dimensional motion patterns of the left ventricle.

The pattern of displacements in the left ventricle (LV) can be described by 13 modes of motion and deformation. Three functional modes of deformation are essential for ejection: a decrease in cavity volume, torsion, and ellipticalization. Four additional modes are used to describe asymmetric deformation. Six modes of rigid body motion describe rotation and translation. In the LV 14-20 radiopaque markers were inserted in the wall of the LV. They were distributed more or less evenly from base to apex and around the circumference. Torsion and volume changes require the definition of a cardiac coordinate system. The point at which ejection focuses is used as the origin, and the torsion axis is used as the z-axis. In the present study the coordinate system was positioned objectively by a least squares fit of the kinematic model to the measured motion of markers. In five dogs in the control state the kinematic parameters were determined as a function of time for all 13 modes. The torsion axis was displaced 4 +/- 2 mm (mean +/- sd) from the center of the cross-section of the LV towards the lateral free wall. The direction of the torsion axis closely coincided with anatomical landmarks at the apex and base. During systole, a unique relation was found between the ratio of cavity volume to wall volume and torsion. This relation was universal to all LVs, the cylinder-symmetric mathematical model of cardiac mechanics inclusive. In diastole the patterns of deformation seem less universal and reproducible.

Animals↗

PubMed1993

Influence of dextrans on platelet distribution in arterioles and venules.

Dextrans bind to the surface of platelets, red blood cells and endothelium. We investigated whether a low doses (30 mg/kg IV) of 40-kDa (Dx40), neutral, 500-kDa (Dx500) or sulphated, 500-kDa (Dx500S) dextrans influence platelet distribution in rabbit mesenteric arterioles and venules (diameter 17-33 microns). Intravital fluorescence videomicroscopy was used to visualize platelets labelled in vivo with acridine red. Their concentration distribution determined within a thin optical section about the median vessel plane was expressed relative to the mean concentration in that vessel. In arterioles, Dx500 and Dx500S increased the relative platelet concentration in the centre [radial position (R): 0.0-0.4 R] from 0.60 to 1.07 (P < 0.001) and 1.20 (P < 0.003), and reduced it near the wall (0.8-0.9 R) from 1.59 to 0.93 (P < 0.02) and 0.95 (P < 0.03) respectively. In venules a similar, but non-significant, effect was observed. Dx40 did not change platelet distribution in arterioles, but decreased their concentration in venules in the centre from 1.08 to 0.71 (P < 0.03) and increased it at the wall from 0.89 to 1.27 (P < 0.04). The deformability of red blood cells was unchanged, but their aggregation tendency increased approximately two-fold after Dx500 and Dx500S injection, while Dx40 had no influence. Leucocyte margination in venules did not affect platelet distribution. Dextran injection did not change microvascular flow velocity or plasma viscosity, suggesting that the observed changes in arteriolar platelet distribution were caused by binding of dextran to the surface of platelets and/or red blood cells.

Animals↗

PubMed1993

Relation between regional electrical activation time and subepicardial fiber strain in the canine left ventricle.

To determine the relation between regional electrical activation time and fiber strain, epicardial electrical activation and deformation were measured in six open-chest dogs at the left ventricular anterior free wall after 15 min of right atrial, left ventricular free wall, left ventricular apex, or right ventricular outflow tract pacing, when end-diastolic pressure was normal or elevated (volume-loading). Regional electrical activation was measured using a 192-electrode brush. Regional subepicardial fiber strain (ef) was measured simultaneously in 16 regions, using optical markers which were attached to the epicardial surface and recorded on video. When relating regional ef during the ejection phase to regional activation time, the best correlation was found when a hemodynamic time reference rather than an electrophysiological one is used. Using the moment of the maximum rate of change of left ventricular pressure as the time reference for electrical activation, regional electrical activation time (t(ea)) and the degree of ef during the ejection phase could be fitted by a linear regression equation ef = a t(ea) + b, in which a = -3.46 +/- 0.73 s-1 an b = -0.28 +/- 0.05. For electrical activation times ranging from -40 to -80 ms, fiber strain was estimated with an accuracy of +/- 0.026 (+/- SE) with this relation. During right atrial pacing, t(ea) and ef were on the average -48 ms and -0.10 respectively. On further investigation, the relation between ef and t(ea) appeared to be influenced by end-diastolic pressure. For normal (1.1 kPa) and elevated end-diastolic pressure (1.8 kPa), the slope of the linear regression line was -3.96 and -2.86 s-1, respectively. Three conclusions may be drawn. Firstly, the time interval between the moment of regional electrical activation and the moment of the maximum rate of change of left ventricular pressure is an index of regional fiber strain. Secondly, it can be concluded from the above equations that electrical asynchrony of more than 30 ms causes non-uniformities in the degree of ef of the order of mean ef during pacing from the right atrium. Finally, differences in fiber strain during asynchronous electrical activation are less pronounced at larger filling pressures.

Animals↗

PubMed1993

Extrapolation of incomplete marker tracks by lower rank approximation.

Motion and deformation of an object such as the heart may be measured by tracking optical or radiopaque markers. In the experimental situation markers may fail to be detected due to occlusion or lack of contrast. As a result a continuous marker track is observed in separated parts, which often cannot be directly identified as corresponding to one marker. This paper presents a method of extrapolating a partly known track by using information provided by the known track part and the available complete tracks of other markers. The extrapolations are obtained by iteratively fitting a lower rank matrix to the set of noisy, incomplete marker tracks. The performance is evaluated with computer-simulated data and data obtained in an animal experiment. In both cases 43% of the available complete tracks were made incomplete by removal of track parts varying in length from 3% up to 44%. For the simulated data comparison of the extrapolations with true signal values results in a root mean square (RMS) error about equal to the noise level. For the animal experiment, when comparing the extrapolations with the measured values, in images of 256 x 256 pixels, the RMS error was found to be +/- 0.5 pixel, which is quite small relative to the total excursion of a marker (20 pixels). Estimation of the missing data by applying BMDPAM (BMDP Statistical Software Inc.) to the same data results in RMS errors which are about twice as high.

Algorithms↗

PubMed1993

Comparison of the performance of the RF cross correlation and Doppler autocorrelation technique to estimate the mean velocity of simulated ultrasound signals.

In pulsed Doppler systems the received RF (radio frequency) signal is multiplied by a quadrature reference signal and subsequently averaged over a short depth range to obtain a sample of the complex Doppler signal. The mean frequency of the sampled Doppler signal, obtained with the autocorrelation function, reflects the mean velocity of the scatterers moving through the sample volume. An alternative is to evaluate the two-dimensional cross correlation function of a short segment of the RF signals over subsequent lines, giving the mean velocity of the scatterers. Both methods of velocity estimation were applied to computer-generated RF signals with varying RF bandwidth, signal-to-noise ratio, and mean and width of the imposed velocity distribution. The length of the RF signal segment and the number of lines for velocity estimation (package length) affects the accuracy of the velocity estimate. It can be concluded that the cross correlation technique behaves superiorly especially for a low velocity dispersion. Furthermore, the standard deviation of the velocity estimate decreases for an increasing sample volume length and package length, while the performance of the conventional Doppler technique is rather independent of the length of the sample volume. The difference between both techniques decreases for a greater package length or for signals simulating a wide velocity distribution.

Algorithms↗

PubMed1993

Short- and long-term effects of smoking on arterial wall properties in habitual smokers.

OBJECTIVES: This study investigated the short-term effects of smoking on hemodynamic function and distensibility and compliance of large arteries in habitual smokers. In addition, the effect of smoking was not measured in nonsmokers, but vessel wall properties were compared between smokers and nonsmokers (basal state). BACKGROUND: Smoking is a well known risk factor for atherosclerosis. Loss of distensibility and compliance of large arteries may play a role in the onset of atherosclerosis. METHODS: The distensibility and compliance coefficients of the common carotid and brachial arteries were determined from the arterial wall displacement during systole and the end-diastolic diameter by using a vessel wall movement detector and from the pulse pressure as assessed in the upper arm. Cardiac function (cardiac output, stroke volume) was measured with Doppler echocardiography. Systemic vascular resistance was calculated as mean arterial pressure divided by cardiac output. RESULTS: In habitual smokers, smoking one cigarette caused a sharp increase in blood pressure (6%) and heart rate (14%). Cardiac index increased (16%), mainly because of the marked increase in heart rate. Stroke and systemic vascular resistance indexes did not change significantly. Smoking enhanced forearm blood flow after wrist occlusion (17%), but total forearm blood flow was unchanged, suggesting an increase in muscle blood flow and a decrease in skin flow. Because of higher blood pressure, the diameter of the elastic common carotid artery increased by 3% (passive phenomenon). Distensibility of the carotid artery decreased (7%), and as a result, carotid compliance was preserved. In contrast, despite higher blood pressure, the diameter of the muscular brachial artery did not change, suggesting an increased vascular tone. Brachial distensibility and compliance decreased (18% and 19%, respectively). Habitual smokers were comparable to nonsmokers with regard to blood pressure, cardiac function, vascular resistance and vessel wall properties of large arteries. Heart rate was higher in habitual smokers (14%). CONCLUSIONS: These data indicate that in habitual smokers, smoking one cigarette causes short-term increases in arterial wall stiffness that might be harmful to the artery and increase the risk for plaque rupture. Except for a higher heart rate, no obvious long-term effect of smoking was observed on hemodynamic variables and arterial stiffness. Because acute cardiovascular events are mainly due to plaque rupture, the short-term effects of smoking might be a more important risk than long-term effects for these acute ischemic events.

Adult↗

PubMed1993

Skin microcirculation in diabetic and non-diabetic patients at different stages of lower limb ischaemia.

One hundred and one non-diabetic and 54 diabetic patients suffering from lower limb ischaemia were divided into (i) asymptomatic subjects, (ii) claudicants, (iii) critically ischaemic patients, i.e. Fontaine III or IV patients with either an ankle pressure < 51 mmHg or a toe pressure < 31 mmHg, and (iv) Fontaine III or IV patients in whom ankle and toe pressures could not be assessed due to vessel wall sclerosis or skin ulceration. Skin microcirculation was investigated to assess (a) the compounding effect of diabetes in leg ischaemia and (b) the additive value of microcirculatory investigation in the appreciation of the severity of the ischaemic disease. The techniques used included capillary microscopy, transcutaneous oximetry and laser Doppler fluxmetry. The severity of ischaemia was readily discernable using microcirculatory techniques. The presence of diabetes appeared to change skin microcirculatory perfusion, but especially in critically ischaemic patients, the microcirculation was no more compromised than non-diabetics. Using skin oxygen tension measurements, a positive predictive value of 77% was obtained in the detection of critical ischaemia, when a cut-off value of 30 mmHg was applied. Seventy per cent of patients, in whom the severity of ischaemia could not be classified using blood pressure measurements, could be classified as critically ischaemic on the basis of microcirculatory investigation. In conclusion, the influence of diabetes on the microcirculation is outweighed by the effects of atherosclerosis when vascular disease becomes severe. Techniques to investigate skin microcirculation are a useful way of assessing the severity of lower limb ischaemia in the presence of diabetes mellitus or if peripheral blood pressures cannot be obtained.

Aged↗