Blood Flow In Microvessels Research Articles

The application of speckle interferometry for the monitoring of blood and lymph flow in microvessels

This paper presents a brief overview of several techniques developed for the analysis of blood microcirculation in vivo. Both theoretical and experimental investigations have been performed using focused Gaussian beams, which are diffracted by blood capillaries with diameters slightly larger than the erythrocyte. Speckle interferometry, utilizing the diffraction of a focused Gaussian beam, was used for the analysis of lymph circulation in native microvessels. The spectra of scattered intensity fluctuations produced by diffraction in such capillaries are analysed, and variations in the envelope of the spectra induced by the influence of drugs on the lymph vessels have also been studied.

Effect of irregularities of vessel cross-section on vascular resistance

Irregularities of the vessel luminal geometry affect resistance to blood flow in microvessels. In the present study, the effect of the protrusion of endothelial cell nuclei into the vessel lumen on vascular resistance is numerically evaluated. It is assumed that nuclei of endothelial cells protrude regularly into the vessel lumen, which has an otherwise circular cross-section. The flow of an incompressible Newtonian fluid in these vessels is numerically analyzed by a finite element method applied to the Stokes equations, and the relationship of the flow rate and the pressure drop between upstream and downstream is used to calculate vascular resistance. It is found that the vascular resistance is constantly elevated compared to that for vessels without protrusions. The vascular resistance increases as the area of the vessel cross-section decreases, its shape is more distorted from the circular, or its variation along the vessel axis is more significant.

Relative Blood Velocity Measurement in Individual Microvessels Using the Self-Mixing Effect in a Fiber-Coupled Helium-Neon Laser

A system has been developed for the measurement of relative blood velocity in microvessels by using the self-mixing effect of a laser. A helium-neon laser was coupled to a single-mode optical fiber and the pulled fiber tip (∼30 μm diameter) was positioned on a single microvessel. The backscattered Doppler-shifted laser light from moving red blood cells enters the laser cavity and modulates the laser output by influencing internal laser parameters. The signal of the laser output intensity change was produced using a fiber-coupled photodiode and processed by a signal processor. This processor yields an output signal proportional to the first moment of the power spectral density, i.e., the mean frequency of the Doppler shift, corresponding to the blood flow velocity on an arbitrary instrument scale. Results of the in vitro experiment demonstrated that the current method can detect moving particles in fluid and moving red blood cells in a small plastic tube. Data from the in vivo study showed that this system is capable of measuring relative blood velocity in arterioles and venules and can easily follow the cardiac cycle up to 360 beats/min. Primary data suggest that, in addition to high sensitivity, good spatial and temporal resolution, and convenience of use, the self-mixing technique may have an even greater capacity for analysis of blood flow in microvessels than explored in this study, since information on the absolute velocity and velocity distribution of red blood cells is available in self-mixing signal. Further study on its hematocrit dependence and particle bias effect is needed.

Resistance to blood flow in microvessels in vivo.

Resistance to blood flow through peripheral vascular beds strongly influences cardiovascular function and transport to tissue. For a given vascular architecture, flow resistance is determined by the rheological behavior of blood flowing through microvessels. A new approach for calculating the contribution of blood rheology to microvascular flow resistance is presented. Morphology (diameter and length), flow velocity, hematocrit, and topological position were determined for all vessel segments (up to 913) of terminal microcirculatory networks in the rat mesentery by intravital microscopy. Flow velocity and hematocrit were also predicted from mathematical flow simulations, in which the assumed dependence of flow resistance on diameter, hematocrit, and shear rate was optimized to minimize the deviation between measured and predicted values. For microvessels with diameters below approximately 40 microns, the resulting flow resistances are markedly higher and show a stronger dependence on hematocrit than previously estimated from measurements of blood flow in narrow glass tubes. For example, flow resistance in 10-microns microvessels at normal hematocrit is found to exceed that of a corresponding glass tube by a factor of approximately 4. In separate experiments, flow resistance of microvascular networks was estimated from direct measurements of total pressure drop and volume flow, at systemic hematocrits intentionally varied from 0.08 to 0.68. The results agree closely with predictions based on the above-optimized resistance but not with predictions based on glass-tube data. The unexpectedly high flow resistance in small microvessels may be related to interactions between blood components and the inner vessel surface that do not occur in smooth-walled tubes.

Red blood cell aggregability is enhanced by physiological levels of hydrostatic pressure

The effect of hydrostatic pressure of up to 15 bars on the aggregability of rat and human red blood cells (RBC), i.e., their capability to form aggregates, was studied using computerized image analysis. The aggregate size distribution was determined under ambient pressure, following application of hydrostatic pressure for various durations up to 2 h. It was found that RBC aggregability markedly increases, up to three-fold, as the pressure which had been applied was increased. Accordingly, higher shear stress is required for dispersing the aggregates of pressure-treated RBC than those of untreated cells. The median size of human RBC aggregates was about three times higher than that of rat RBC, and this ratio was maintained following pressure treatment. RBC aggregability is a major determinant in blood flow, especially in the microcirculation. Pressure at the levels used in this study occurs in physiological states such as hyperbaric treatment or diving. The enhanced aggregability induced by application of such pressure implies that blood flow in microvessels might be altered under conditions associated with elevated hydrostatic pressure.

Malaria, the red cell, and the endothelium.

Erythrocytes infected with mature stages of Plasmodium falciparum malaria adhere to vascular endothelial cells in postcapillary venules of several organs. In some patients, infected cells also form rosettes with uninfected erythrocytes. The special pathology of acute cerebral malaria appears to result from excessive adherence of infected cells in cerebral vessels coupled with occlusion of cerebral blood flow in microvessels by infected cell rosettes. Several endothelial cell proteins have been identified as potential receptors for infected erythrocyte adherence to vascular endothelium, including thrombospondin, CD36, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1). The receptor on infected erythrocytes that mediates adhesion to endothelial cells has been identified as a very large malarial protein on infected cells called PfEMP1. PfEMP1 has been shown to bind to CD36 and thrombospondin in vitro. Antibody-mediated blockade or reversal of infected erythrocyte adherence to vascular endothelium is postulated not only to decrease the pathology of blood-stage malaria, but also to lead to infected cell destruction and clearance, especially in the spleen. PfEMP1 is therefore a prime candidate malarial protein for inclusion in a multicomponent asexual malaria vaccine.

Regional differences in microvascular response in rat intestine during acute elevation of portal pressure.

The effect of acute elevation of portal pressure on the blood flow of rat intestinal microvessels was studied using a laser Doppler velocimeter and in vivo microscopy. The total intestinal blood flow decreased when portal pressure increased more than +15 cmH2O above the basal value. Blood flow in villus capillaries did not change at portal pressures of +5 to +15 cmH2O, but did decrease at +20 cmH2O. Blood flow in muscle capillaries decreased at all steps of portal hypertension. Red blood cell velocity was decreased by portal hypertension in large venules, but not in small venules of the submucosa. Large venules, but not small venules, dilated in acute portal hypertension. Large arterioles in the submucosa constricted, while small arterioles dilated at portal pressures of +10 to +15 cmH2O. In conclusion, the intestinal microvascular flow response differs according to the degree of portal hypertension and the location on the microvascular tree. Blood flow in villus capillaries and in small submucosal venules is maintained at a small degree of portal hypertension.

Plasmodium falciparum-infected erythrocytes do not adhere well to C32 melanoma cells or CD36 unless rosettes with uninfected erythrocytes are first disrupted.

Plasmodium falciparum malaria parasites modify the human erythrocytes in which they grow so that some parasitized erythrocytes (PE) can cytoadhere (C+) to host vascular endothelial cells or adhere in rosettes (R+) to uninfected erythrocytes. These C+ and R+ adherence properties of PE appear to mediate much of the pathogenesis of severe malaria infections, in part by blocking blood flow in microvessels. From one parasite strain, PE were selected in vitro for C+ R+ or C+ R- adherence properties and examined in model adherence assays. The C+ R+ PE cytoadhered poorly to C32 melanoma cells or to immobilized CD36 in a settled-cell assay when uninfected human erythrocytes were present and formed rosettes with PE. C+ R- PE adhered well in the same assays. However, C+ R+ PE adhered very well, even better than C+ R- PE, when the rosettes were disrupted and the C+ R+ PE were purified. Adding back rabbit erythrocytes, which do not form rosettes with C+ R+ PE, had simply a dilutional effect. The ability of rosettes to interfere with the detection of adherence must be dealt with in all future assays of malarial PE adherence. Individual PE were observed attached simultaneously to C32 cells and to a few erythrocytes, suggesting that C+ and R+ adherence properties are coexpressed on the same PE. Coexpression of these adherence properties on the same PE may have pathological importance in vivo, where passage of rosettes through capillaries may shear uninfected erythrocytes from rosetted PE and allow direct PE attachment to postcapillary venule walls before rosettes reform.

Spiral optical-frequency shifter for lower-velocity measurement of the laser Doppler velocimeter

A spiral optical-frequency shifter for the laser Doppler velocimeter (LDV) is described, which offers lower shifted frequencies of 50 Hz–50 kHz manually. These lower shifted frequencies cannot be easily obtained from conventional optical-frequency shifters (Bragg cell, rotating diffracting grating, etc.). However, these lower shifted frequencies are useful for LDV measurement of lower-velocity flow such as blood flow in microvessels. A spiral optical element consisting of acrylic resin (refractive index, n=1.61) is inserted into one of the dual incident beams of a differential LDV, in which an optical frequency shift is brought about by rotation of the spiral element. The shifted frequency is changed by rotational frequency mechanically. The performance of the shifter is discussed; the experimental results are in good agreement with the theoretical values of shifted frequencies (error <1%).

The control of macro- and microcirculation in the mesentery and intestine.

The total blood flow and microvessel blood flow in the mesentery and the intestine anesthetized rabbits were measured while systemic hemodynamics were altered by baroreceptor stimulation and by noradrenaline injection. The percent change of the total peripheral resistance (Rt) was greater than the change in resistance in the intestinal vascular bed (Ri) during baroreceptor stimulation. The capillary blood flow in the intestinal muscle layer (Qs) and villus (Qv) increased slightly while the intestinal arterial flow (Qa) and the arteriolar flow in the mesentery (Qm) decreased. These data indicated that Qs and Qv were not controlled by the sympathetic vasoconstrictor system. The percent change of Ri was greater than that of Rt during noradrenaline injection. Noradrenaline decreased Qa, but Qs and Qv were decreased while Qm was increased. These results show that noradrenaline stimulates alpha-adrenoceptors on small arteries and arterioles in the intestine. The observed Qm changed was in response to the systemic hemodynamic change caused either by the baroreceptor input or by noradrenaline.

The dynamic analysis of the vasomotion in microcirculation

The vasomotion of the microcirculation which has been observed in experiments are studied with a simple model of the fluid dynamics. The influence of the vasomotion on the blood flow in microvessels is analysed and the streamlines, velocity and pressure distribution and the variation of the flow rate are presented.

Velocity profiles of blood flow in microvessels measured by ten channels' dual-sensor method.

Ten channels' dual-sensor method newly developed was applied to the measurement of velocity profiles in arterioles and venules in the rat mesentery. In some experiments, red blood cells (RBC), labelled in vitro with a fluorescein isothiocyanate (FITC), were injected to compare the velocity profiles obtained by the RBC visualization technique with those measured by the dual-sensor method. It was found that the velocity profile of the FITC labelled RBC in straight microvessels was blunt as compared to a parabola. The centerline velocity measured by the dual-sensor method was smaller than that of the FITC labelled RBC by about 20%. The velocity profiles were also measured at the curved arterioles and venules as well as at the bifurcation and the confluence. It was found that the velocities were higher along the inner wall at the curved portion and along the outer wall at the bifurcation of arterioles.

Influence of Plasma Layer on Steady Blood Flow in Microvessels

A semi-empirical new model for steady blood flow in microvessels is proposed. In the model, a peripheral layer devoid of blood cells (called the plasma layer) is taken into account and the central core of blood surrounded by the plasma layer is assumed to obey the Herschel-Bulkley equation. The velocity distribution and the pressure-flow relation have been derived for the model. To study the rheological condition of the blood flow in arterioles, the model is compared with the experimental data obtained by Einav et al., using the Laser Doppler anemometry. It is found that the experimental data for velocity profiles are explained fairly well by this model, if appropriate values are chosen for parameters. A careful investigation of these data reveals that the blood flow in microvessels can be regarded apparently as a Newtonian flow owing to the presence of the plasma layer.

Mechanisms of blood flow and fluid exchange in microvessels: hemorrhagic hypotension model.

Mechanisms of blood flow and fluid exchange in microvessels: hemorrhagic hypotension model.

Blood pressure, flow, and elastic properties in microvessels of cat omentum.

ARTICLESBlood pressure, flow, and elastic properties in microvessels of cat omentumM Intaglietta, DR Richardson, and WR TompkinsM Intaglietta, DR Richardson, and WR TompkinsPublished Online:01 Sep 1971https://doi.org/10.1152/ajplegacy.1971.221.3.922MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPEG-albumin supraplasma expansion is due to increased vessel wall shear stress induced by blood viscosity shear thinningKrishna Sriram, Amy G. Tsai, Pedro Cabrales, Fantao Meng, Seetharama A. Acharya, Daniel M. Tartakovsky, and Marcos Intaglietta15 June 2012 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 302, No. 12In vivo two-photon excited fluorescence microscopy reveals cardiac- and respiration-dependent pulsatile blood flow in cortical blood vessels in miceThom P. Santisakultarm, Nathan R. Cornelius, Nozomi Nishimura, Andrew I. Schafer, Richard T. Silver, Peter C. Doerschuk, William L. Olbricht, and Chris B. Schaffer1 April 2012 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 302, No. 7Temporal and spatial variations of cell-free layer width in arteriolesSangho Kim, Robert L. Kong, Aleksander S. Popel, Marcos Intaglietta, and Paul C. Johnson1 September 2007 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 293, No. 3Onset of pulsatile pressure causes transiently increased filtration through artery wallJonathan P. Alberding, Ann L. Baldwin, Jennifer K. Barton, and Elizabeth Wiley1 May 2004 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 286, No. 5 More from this issue > Volume 221Issue 3September 1971Pages 922-928 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.221.3.922PubMed5570351History Published online 1 September 1971 Published in print 1 September 1971 Metrics