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H H Lipowsky

Publications and source records attributed to H H Lipowsky.

At least 37 records · Page 2Linked to original sources
PubMed1988

Arteriovenous distribution of transit times in cremaster muscle of the rat.

Video digitization was applied to determine the arteriovenous transit time (TT) of blood flow between functionally paired arterioles and venules in cremaster muscle (rat). After a bolus injection of cell-free dye (FITC-Dextran) into a contralateral femoral artery, intensity-time curves (ITCs) of the fluorescent emissions were recorded in successive network divisions. TTs were calculated by cross-correlation of ITCs acquired from the video images digitized at rates of 5-10 frames/sec for up to 10 arteriole-venule (AV) pairs per video field whose position in the network was characterized in terms of centrifugal order of branching. Mean TT for first-order AV pairs averaged 3.74 +/- 1.62 (SD) sec and decreased significantly to 0.76 +/- 0.95 sec in the fifth-order pairs, with 75% of this reduction occurring between the first- and third-order pairs. A near threefold increase in coefficient of variation from first to fifth orders evidenced a marked increase in the spatial heterogeneity of TT at the level of the true capillaries. Comparison of TT with distance along the arterial tree from the tissue hilus revealed consistently stronger correlations than with AV order. These trends suggest that TT may be a superior indicator of the functional deployment of microvessels compared to branching order.

Animals↗
PubMed1988

In vivo determination of the force of leukocyte-endothelium adhesion in the mesenteric microvasculature of the cat.

Quantitative estimates of the force of adhesion between leukocytes and endothelium were obtained from in vivo hemodynamic measurements in small venules of cat mesentery during topical application of the chemotactic compound N-formyl-methionyl-leucyl-phenylalanine (FMLP). Simultaneous measurements of upstream to downstream pressure drop, red cell velocity, microvessel hematocrit, and vessel diameter and length permitted application of the principles of momentum conservation to calculate the forces acting upon a leukocyte during adhesion to the endothelium. For venules ranging in diameter from 23 to 49 micron, the ratio of force (acting in the vessel axial direction) to wall shear stress on the endothelium fell from 14.6 X 10(-6) in small venules to 2.3 X 10(-6) dynes per dyne/cm2 in large venules; reflecting the larger pressure drops and forces attendant to greater lumen obstruction in the smaller venules. The equilibrium force representative of a balance between fluid shear stresses on the leukocyte and those at its site of contact with the endothelium ranged from 1.1 to 76.1 X 10(-5) dynes for wall shear stress ranging from 2 to 25 dynes/cm2; with venules with greater wall shear stresses having the greater leukocyte-endothelium shear force. Within individual venules, however, the force acting on a single leukocyte varied inversely with wall shear stress, most likely due to white blood cell deformation, which leads to a lessening of shear stress on the surface of the white blood cell.

Animals↗
PubMed1987

Leukocyte-endothelium adhesion: microhemodynamics in mesentery of the cat.

The effects of leukocyte-endothelium adhesion on microhemodynamics were studied in cat mesentery under control conditions and following tissue suffusion with the chemotactic agent N-formyl-methionyl-leucyl-phenylalanine (FMLP). The results indicate that under normophysiological conditions there is little or no leukocyte-endothelium adhesion in arterioles and venules. Tissue suffusion with FMLP significantly increases the number of adhering leukocytes in venules, but not in arterioles. Analysis of the number of adhering leukocytes (in venules) as a function of wall shear rate suggested that increased adhesion of leukocytes was primarily due to elevated adhesive forces and not the result of decreases in dispersal forces, i.e., wall shear stress. From measurements of upstream to downstream pressure drop, red cell velocity, and microvessel hematocrit in 16 unbranched venules, no significant changes in diameter (mean of 39.9 +/- 7.8 (SD) micron), intravascular pressure gradient (0.59 +/- 0.40 X 10(-2) cm H2O/micron), nor microvessel hematocrit (31.0 +/- 9.8%) occurred in response to FMLP. There were significant decreases in upstream pressure (8%) and estimated bulk flow (28%) as well as significant increases in the number of adhering leukocytes, from 1.5 +/- 2.8 to 11.4 +/- 8.3 cells/100 micron, and vessel resistance (81%). Changes in hemodynamics were found to be more pronounced in venules with small diameters. The observed response to FMLP suggests that changes in hemodynamics during leukocyte-endothelium adhesion can be accounted for by a decrease in the effective diameter due to obstruction of the lumen by WBCs, and that adhesive interactions between WBCs and endothelium are a major determinant of blood flow resistance in the microcirculation.

Animals↗
PubMed1987

Microvascular hematocrit and red cell flux in rat cremaster muscle.

The arteriovenous distributions of volumetric flow (Q), microvessel hematocrit (Hctmicro), and estimates of red cell volumetric flux (QRBC) were obtained under control conditions in rat cremaster muscle. The results demonstrate a monotonic fall in the ratio of Hctmicro/Hctsystemic from 0.86 in 70-microns arterioles to 0.48 in capillaries followed by a subsequent rise to 0.79 in 98-microns venules. To assess the roles of Hctmicro and Q in red blood cell delivery following a period of reduced oxygen transport, tissue ischemia was produced by occluding the first order arteriole. During the occlusion, arteriolar and large venular hematocrits fell 15-30%, whereas small venular hematocrits increased 24%. After release of the occlusion, a reactive hyperemia ensued with Q, QRBC, and QHctmicro increasing significantly above control values in arterioles, capillaries, and venules. All Hctmicro returned to their control values within 10 s following resumption of flow. Based on the relationship between blood viscosity and Hctmicro, at low shear rate, these transient alterations in Hctmicro were estimated to have a profound effect on blood viscosity, and hence the resistance to blood flow. Such changes may affect recovery from an ischemic episode, although not adversely affecting the oxygen-carrying capacity of blood and convective transport of oxygen.

Animals↗
PubMed1987

Intravital microscopy of capillary hemodynamics in sickle cell disease.

Direct intravital microscopic examinations were made in nailfold capillaries in subjects with homozygous sickle cell disease (HbSS red cells). In the resting state, capillary red cell (rbc) flux exhibited greater intermittence compared with normal subjects, which increased with painful crisis. In crisis-free HbSS subjects, capillary occlusion and red cell sequestration occurred in only 8.2% of all capillaries and diminished to 5.8% during crisis, possibly due to sequestration of less deformable rbcs in other organs. Velocities of rbc's (Vrbc) were measured by video techniques under resting conditions and during postocclusive reactive hyperemia (PORH) induced by a pressure cuff around the finger. Resting Vrbc was normal in crisis-free HbSS subjects, averaging 0.7 mm/s. In contrast, Vrbc was significantly elevated during crisis, to 0.98 mm/s, apparently due to compensatory arteriolar dilation. Crisis subjects exhibited a significantly depressed PORH with the ratio of peak red cell velocity to resting values reduced by 15% due to a loss of vasodilatory reserve, whereas crisis-free subjects exhibited a normal response. A 55% increase in the time to attain peak Vrbc was attributed to resistance increases, possibly resulting from red cell and leukocyte-to-endothelium adhesion during the induced ischemia.

Adult↗
PubMed1987

Rheology of sickle cells and its role in microcirculatory dynamics.

The alterations in the viscoelastic properties of the hemoglobin S solution following deoxygenation can be correlated, on the one hand, with the gelation of the HbS molecules and, on the other hand, with changes in the rheological behavior of the deoxygenated SS erythrocytes. The abnormal rheology of SS erythrocytes forms the basis of their altered flow behavior through filter pores in vitro and microcirculation in vivo. The results support the notion that the rheological behavior of sickle cells is an important link between the molecular events in hemoglobin S following deoxygenation and the behavior of the cell in the microcirculation. Although recent advances have shed considerable lights on the rheology of sickle cells in a variety of conditions, further studies are needed in order to elucidate the pathophysiological role of cell rheology in this disease, especially in terms of the influence of individual SS cells in the heterogeneous populations and the correlation between in vitro and in vivo behavior of SS cells.

Anemia, Sickle Cell↗
PubMed1986

Microvascular hemodynamics during systemic hemodilution and hemoconcentration.

Measurements of intravascular pressure, red blood cell (RBC) velocity, and microvessel hematocrit (Hctmicro) were made in arterioles and venules of the cat mesenteric microvasculature during systemic hemodilution (cell-free plasma) and hemoconcentration (packed cells). For a range of systemic hematocrits (Hctsys) from 5 to 67%, changes in volumetric flux of red cells (QRBC) were derived from the product of microvessel bulk flow and Hctmicro. During hemodilution, a heterogeneous response of changes in QRBC was found with larger distributing arterioles (43-54 microns) exhibiting a monotonic fall, whereas increases in QRBC above control were found in smaller arterioles that were indicative of a potential enhancement of oxygen delivery. Although the dilution response of all arterioles and venules averaged for all calibers of vessels demonstrated a decline in QRBC, alterations of Hctmicro suggested a lessening of the disparity between Hctsys and Hctmicro, which was indicative of a more efficient utilization of the remaining circulating RBC volume. In response to hemoconcentration, a decrease in QRBC also occurred, which, in concert with the dilution data, suggested that QRBC was maximized for a range of 28 less than Hctsys less than 46%. From measurements of the arteriovenous pressure drop across mesenteric modules, regional resistance was found to exhibit a relative plateau as Hctsys was increased above its control value. This behavior was attributed to a decrease in vascular hindrance of the principal resistance vessels and an invariance of blood viscosity at the capillary level due to RBC redistribution and the attendant viscous behavior of blood.

Animals↗
PubMed1985

A model of microvascular oxygen transport in sickle cell disease.

The model of local control of oxygen delivery in the microvasculature developed by H. J. Granger and A. P. Shepherd (1973, Microvasc. Res. 5, 49-72) was extended to describe microcirculatory blood flow in sickle cell disease. Two major characteristics of sickle cell blood were incorporated into the model: an abnormal blood viscosity which is dependent on the degree of hemoglobin oxygen saturation and hematocrit, and a reduced affinity of hemoglobin (Hb) for oxygen. Sickle cell blood viscosity as a function of oxygen saturation and hematocrit was modeled empirically based upon existing data. Alterations in HbO2 affinity were studied in the model by introducing P50 as an independent variable. The altered oxygen supply/demand relationship in sickle cell disease was simulated following an increase in tissue metabolic demand and a decrease in arteriolar blood flow. The results were analyzed to evaluate the roles of the various rheological characteristics of sickle cell blood in affecting microcirculatory dynamics and tissue oxygen delivery. It was demonstrated that, within the hematocrit range of 20 to 45%, the elevation of P50 from 27 to 38 mm Hg in sickle cell blood is adequate to compensate for the diminished O2 content, despite an elevated blood viscosity, and maintain near normal tissue pO2.

Anemia, Sickle Cell↗
PubMed1984

Arteriovenous distribution of hemodynamic parameters in the rat dental pulp.

A systematic investigation of the distribution of red cell velocity throughout the hierachy of the rat pulp microvascular network was performed. Luminal diameters (D) of microvessels ranging in size from 8 to 72 micron were measured in situ by an electronic video image shearing technique. Intravascular red cell velocities (Vrbc) were simultaneously measured by a variation of the "two-slit" photometric technique and intravascular volumetric flow rates (Q) were calculated. It was found that red cell velocity decreased monotonically throughout successive arteriolar divisions to attain capillary values of 1/10 those in the feeding arterioles. A slight rise in Vrbc was found in the venous confluences, however, a maximum value of Vrbc of only 1/5 large arteriolar values was evident in the large collecting venules. In contrast, the calculated volumetric flow rate distribution was found to be nearly parabolic from arterioles (40 micron) and their paired (72 micron) collecting venules. This behavior was attributed to the dominance of microvessel cross-sectional areas as a determinant of Q.

Animals↗
PubMed1984

Segmental and total microvascular resistances during hemorrhagic hypotension in rabbit omentum.

Single input-output microvascular modules in the rabbit omentum were studied to quantitate total modular resistance (RT) and the changes in resistance of successive serial segments (Rseg) during hemorrhagic hypotension (55 mmHg for 1 h). RT was calculated from the pressure drop between input and output vessels and the total flow through the module. Changes in Rseg were estimated from alterations in single microvessel hindrance (1/diam4) for selected microvessels within a module together with a correction for flow redistribution within each segment derived from changes in the proportion of total flow. Mean RT increased to 2.1 times control within the first 10 min of systemic hypotension and gradually declined over 1 h. Response of Rseg varied in different generations of microvessels (arterioles and venules subdivided by size). Rseg for arterioles and venules less than 30 microns, but not that for arterioles and venules greater than 30 microns, showed comparable or greater changes than RT. Calculated differences between RT and the summed Rseg of measured segments suggest that the unmeasured Rseg in capillaries and blood rheological parameters may have significantly influenced changes in RT during hemorrhagic hypotension.

Animals↗
PubMed1982

Human SS red cell rheological behavior in the microcirculation of cremaster muscle.

The hemodynamic behavior of Hb SS erythrocytes introduced into the microcirculation of cremaster muscle (rat and mouse) was studied by intravital microscopy. Simultaneous measurements of intravascular pressure, pressure drop, red cell velocity, hematocrit and oxygen tensions were made to evaluate both regional resistance (arteriovenous) from 2nd order arterioles to venules, as well as the resistance to blood flow in single unbranched arterioles. Following the isovolemic exchange of 2 to 3 blood volumes with SS cells at 25% hematocrit, regional resistance remained within 20% of its control value due to compensatory vasodilation and shunting of blood through pathways parallel to capillaries occluded by sickled red cells. Prolonged exposure to circulating SS cells resulted in a degradation of microvascular function with an attendant four-fold rise in regional resistance. Transient resistance measurements during the passage of a bolus of SS cells through the cremasteric network demonstrated a 100% increase in regional resistance, which was rapidly abated by the subsequent SS cell washout and capillary recruitment. Computations of apparent viscosity in single unbranched arterioles (nominal diameter of 45 micrometer) revealed a four-fold rise in viscosity following the reduction in intravascular oxygen tension (PO2) from 40 mm HG to 7 mm Hg. Observations on the transient increase in viscosity concomitant with a rapid decrease in PO2, demonstrated a lag time of 2 to 3 s before the elevation of viscosity. To enhance the visualization of these processes, techniques for the fluorescent labelling of Hb SS cells with fluorescein isothiocyanate (FITC) were applied. Visual observations of the movement of SS-FITC red cells by fluorescence microscopy readily revealed the sequestration of sickled cells at the junction between 10 micrometer transverse arterioles and the smaller true capillaries, and the shunting of labelled cells around obstructed capillaries.

Abdominal Muscles↗
PubMed1982

Correlation of hemodynamics in macrocirculation and microcirculation.

The current state of our understanding on the correlation between hemodynamics in the micro- and macrocirculation is assessed. The use of microcirculatory approach has allowed the identification of the sites of microvascular responses to neuro-humoral influences which are known to affect the overall resistance determined by macrocirculatory experimentation. Direct determinations of hematocrit and apparent viscosity in microvessels have helped to interpret macrocirculatory findings on the distribution of red cells and plasma and on the pressure-flow relationships in normal and pathological conditions. Hemodynamic measurements made on microvessels in the ventricular epicardium have provided the microcirculatory bases of the variations in coronary blood flow during the cardiac cycle and the changes in coronary hemodynamics in response to vasodilators. Microcirculatory studies on the surface glomeruli of Munich-Wistar rats have allowed the identification of the sites of microvascular actions of vasoactive agents and the determination of their effects on glomerular filtration coefficient. Several attempts have been made to synthesize the overall hemo-dynamics at the organ level from microcirculatory data, with some degree of success. In order to attain the goal of correlating macrocirculatory and microcirculatory hemo-dynamics, we need to perform parallel investigations at these levels on the same organs or tissues in the same animal species, together with morphological characterization of the microcirculatory architecture and theoretical modeling in which accounts are taken of the heterogeneity of structural and functional parameters.

Animals↗
PubMed1978

The distribution of blood rheological parameters in the microvasculature of cat mesentery.

In vivo studies of the rheological behavior of blood in the microcirculation were conducted by direct in situ measurements in cat mesentery. Upstream to downstream pressure drops were measured in unbranched arterioles, capillaries, and venules, with diameters from 7 to 58 micrometer. Simultaneous measurements of red cell velocity and vessel geometry facilitated computation of bulk velocity, pressure gradient, apparent viscosity, wall shear stress, and resistance. Arteriovenous distributions of these parameters revealed the following. Maximum pressure gradient (0.015 cm H20/micrometer) occurs in the true capillaries (7 micrometer in diameter); intravascular wall shear stress averaged 47.1 dynes/cm2 in arterioles and 29.0 dynes/cm2 in venules. Extreme values as great as 200 dynes/cm2 were observed in a few shunting arterioles. Apparent viscosity averaged 3.59 cP in arterioles, 5.15 cP in venules, and 4.22 cP overall. Intravascular resistance per unit length of microvessel varied with luminal diameter as a power law function with exponents of -4.04 for arterioles, -3.94 for venules, and -3.99 for all vessels combined. This apparent maintenance of Poiseuille's law is attributed to the opposing processes of hematocrit reduction and decreasing shear rate as blood is dispersed in successive arteriolar segments, and the converse action of these processes in the venous confluences which lessen the extent of network variations in apparent viscosity. Reductions in bulk velocity from the normal flow state to below 0.5 mm/sec resulted in increases in apparent viscosity by a factor of 2 to 10, which are attributed primarily to obstruction of the lumen by leukocyte-endothelium adhesion.

Animals↗