Microvascular blood flow resistance: role of endothelial surface layer

1997 ◽  
Vol 273 (5) ◽  
pp. H2272-H2279 ◽  
Author(s):  
Axel R. Pries ◽  
Timothy W. Secomb ◽  
Helfried Jacobs ◽  
Markus Sperandio ◽  
Kurt Osterloh ◽  
...  

Observations of blood flow in microvascular networks have shown that the resistance to blood flow is about twice that expected from studies using narrow glass tubes. The goal of the present study was to test the hypothesis that a macromolecular layer (glycocalyx) lining the endothelial surface contributes to blood flow resistance. Changes in flow resistance in microvascular networks of the rat mesentery were observed with microinfusion of enzymes targeted at oligosaccharide side chains in the glycocalyx. Infusion of heparinase resulted in a sustained decrease in estimated flow resistance of 14–21%, hydrodynamically equivalent to a uniform increase of vessel diameter by ∼1 μm. Infusion of neuraminidase led to accumulation of platelets on the endothelium and doubled flow resistance. Additional experiments in untreated vascular networks in which microvascular blood flow was reduced by partial microocclusion of the feeding arteriole showed a substantial increase of flow resistance at low flow rates (average capillary flow velocities < 100 diameters/s). These observations indicate that the glycocalyx has significant hemodynamic relevance that may increase at low flow rates, possibly because of a shear-dependent variation in glycocalyx thickness.

2013 ◽  
Vol 136 (1) ◽  
Author(s):  
Qing Pan ◽  
Ruofan Wang ◽  
Bettina Reglin ◽  
Guolong Cai ◽  
Jing Yan ◽  
...  

Techniques that model microvascular hemodynamics have been developed for decades. While the physiological significance of pressure pulsatility is acknowledged, most of the microcirculatory models use steady flow approaches. To theoretically study the extent and transmission of pulsatility in microcirculation, dynamic models need to be developed. In this paper, we present a one-dimensional model to describe the dynamic behavior of microvascular blood flow. The model is applied to a microvascular network from a rat mesentery. Intravital microscopy was used to record the morphology and flow velocities in individual vessel segments, and boundaries are defined according to the experimental data. The system of governing equations constituting the model is solved numerically using the discontinuous Galerkin method. An implicit integration scheme is adopted to increase computing efficiency. The model allows the simulation of the dynamic properties of blood flow in microcirculatory networks, including the pressure pulsatility (quantified by a pulsatility index) and pulse wave velocity (PWV). From the main input arteriole to the main output venule, the pulsatility index decreases by 66.7%. PWV obtained along arterioles declines with decreasing diameters, with mean values of 77.16, 25.31, and 8.30 cm/s for diameters of 26.84, 17.46, and 13.33 μm, respectively. These results suggest that the 1D model developed is able to simulate the characteristics of pressure pulsatility and wave propagation in complex microvascular networks.


2005 ◽  
Vol 289 (6) ◽  
pp. H2657-H2664 ◽  
Author(s):  
A. R. Pries ◽  
T. W. Secomb

The apparent viscosity of blood in glass tubes declines with decreasing diameter (Fåhraeus-Lindqvist effect) and exhibits a distinctive minimum at 6–7 μm. However, flow resistance in vivo in small vessels is substantially higher than predicted by in vitro viscosity data. The presence of a thick endothelial surface layer (ESL) has been proposed as the primary cause for this discrepancy. Here, a physical model is proposed for microvascular flow resistance as a function of vessel diameter and hematocrit in vivo; it combines in vitro blood viscosity with effects of a diameter-dependent ESL. The model was developed on the basis of flow distributions observed in three microvascular networks in the rat mesentery with 392, 546, and 383 vessel segments, for which vessel diameters, network architecture, flow velocity, and hematocrit were determined by intravital microscopy. A previously described hemodynamic simulation was used to predict the distributions of flow and hematocrit from the assumed model for effective blood viscosity. The dependence of ESL thickness on vessel diameter was estimated by minimizing deviations of predicted values for velocities, flow directions, and hematocrits from measured data. Optimal results were obtained with a layer thickness of ∼0.8–1 μm for 10- to 40-μm-diameter vessels and declined strongly for smaller diameters, with an additional hematocrit-dependent impact on flow resistance exhibiting a maximum for ∼10-μm-diameter vessels. These results show that flow resistance in vivo can be explained by in vitro blood viscosity and the presence of an ESL and indicate the rheologically effective thickness of the ESL in microvessels.


2021 ◽  
Vol 117 ◽  
pp. 110241
Author(s):  
Alberto Coccarelli ◽  
Supratim Saha ◽  
Tanjeri Purushotham ◽  
K. Arul Prakash ◽  
Perumal Nithiarasu

1996 ◽  
Vol 16 (1_suppl) ◽  
pp. 137-141 ◽  
Author(s):  
Peter Jonasson ◽  
Ulf Bagge ◽  
Anders Wieslander ◽  
Magnus Braide

Data from cell culture experiments indicate that heat sterilization of peritoneal dialysis (PD) fluids produces cytotoxic glucose degradation products. The present vital microscopic study investigated the effects of different sterilization methods on the biocompatibility of PD fluids. Thus, heat-sterilized (commercially obtained and experimentally produced) and filter-sterilized PD fluids (pH = 5.30 5.40; 1.5% glucose) were compared with Tyrode buffer, with respect to the effects on microvascular blood flow velocity and leukocyte adhesion in the rat mesentery. Exteriorization of the mesentery produced a mild inflammation, known from the literature and characterized by the adhesive rolling of leukocytes along venular walls. Superfusion of the mesentery with filter-sterilized PD fluid had no significant effects on leukocyte rolling or flow velocity in venules 25 40 μm in diameter compared with buffer superfusion. Heat-sterilized PD fluid decreased the concentration of rolling leukocytes and increased flow velocity significantly, as compared with buffer and filter-sterilized PD fluid. The results indicate that heat sterilization of PD fluids produces substances that interact with microvascular tone and leukocyte-endothelial adhesion, which hypothetically could impair the acute, granulocyte-mediated defense against bacterial infections.


2001 ◽  
Vol 90 (6) ◽  
pp. 2025-2032 ◽  
Author(s):  
Julian M. Stewart ◽  
Amy Weldon

Dependent pooling occurs in postural orthostatic tachycardia syndrome (POTS) related to defective vasoconstriction. Increased venous pressure (Pv) >20 mmHg occurs in some patients (high Pv) but not others (normal Pv). We compared 22 patients, aged 12–18 yr, with 13 normal controls. Continuous blood pressure and strain-gauge plethysmography were used to measure supine forearm and calf blood flow, resistance, venous compliance, and microvascular filtration, and blood flow and swelling during 70° head-up tilt. Supine, high Pv had normal resistance in arms (26 ± 2 mmHg · ml−1 · 100 ml · min) and legs (34 ± 3 mmHg · ml−1 · 100 ml · min) but low leg blood flow (1.5 ± 0.4 ml · 100 ml−1 · min−1). Supine leg Pv (30 ± 2 vs. 13 ± 1 mmHg in control) exceeded the threshold for edema (isovolumetric pressure = 19 ± 3 mmHg). Supine, normal Pv had high blood flow in arms (4.1 ± 0.2 vs. 3.5 ± 0.2 ml · 100 ml−1 · min−1 in control) and legs (3.8 ± 0.4 vs. 2.7 ± 0.3 ml · 100 ml−1 · min−1 in control) with low resistance. With tilt, calf blood flow increased steadily in POTS with high Pv and transiently increased in normal Pv. Calf volume increased in all POTS patients. Arm blood flow increased in normal Pv only with forearm maintained at heart level. These data suggest that there are (at least) two subgroups of POTS characterized by high Pv and low flow or normal Pv and high flow. These may correspond to abnormalities in local or baroreceptor-mediated vasoconstriction, respectively.


2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Luciana N Torres ◽  
Ivo P Torres Filho ◽  
Roland N Pittman ◽  
Aleksander S Golub

1996 ◽  
Vol 270 (2) ◽  
pp. H545-H553 ◽  
Author(s):  
A. R. Pries ◽  
T. W. Secomb ◽  
P. Gaehtgens

The relationship between structural and hemodynamic heterogeneity of microvascular networks is examined by analyzing the effects of topological and geometric irregularities on network hemodynamics. Microscopic observations of a network in the rat mesentery provided data on length, diameter, and interconnection of all 913 segments. Two idealized network structures were derived from the observed network. In one, the topological structure was made symmetric; in another a further idealization was made by assigning equal lengths and diameters to all segments with topologically equivalent positions in the network. Blood flow through these three networks was simulated with a mathematical model based on experimental information on blood rheology. Overall network conductance and pressure distribution within the network were found to depend strongly on topological heterogeneity and less on geometric heterogeneity. In contrast, mean capillary hematocrit was sensitive to geometric heterogeneity but not to topological heterogeneity. Geometric and topological heterogeneity contributed equally to the dispersion of arteriovenous transit time. Hemodynamic characteristics of heterogeneous microvascular networks can only be adequately described if both topological and geometric variability in network structure are taken into account.


1984 ◽  
Vol 247 (4) ◽  
pp. G339-G345
Author(s):  
S. W. Ashley ◽  
L. Y. Cheung

The validity of the use of H2 gas clearance to measure gastric mucosal blood flow (GMBF) was investigated in the intact stomach of anesthetized dogs. With a modified, more sensitive platinum electrode, we were able to reduce the H2 gas concentration to a nonflammable gas mixture. GMBF was repeatedly measured when the dogs inhaled gas containing 100, 10, and 3-5% H2. GMBF measured using 100% H2 demonstrated close correlation with inhaled gases containing 10% H2 (r = 0.84, slope = 0.89) and 3-5% H2 (r = 0.91, slope = 0.88). At a nonflammable concentration of 3% H2, it was safe to add 20% O2 into the gas mixture. The addition of O2 into the inhaled gas eliminated the transient hypoxia noted otherwise. It was also possible to reduce the gas flow rate from 5-10 to 1-3 l/min. Regression analysis of GMBF determined by inhalation of 5% H2 at these flow rates revealed a significant linear correlation (r = 0.95, slope = 1.13). In 10 dogs GMBF determined by using these low concentrations of H2 at the low flow rates also showed a good agreement (r = 0.93, slope = 0.65) with that measured by radioactive microspheres. These two methods also demonstrated comparable changes in GMBF induced by intravenous infusion of histamine and vasopressin. It was concluded that, with the technique as modified in our laboratory, H2 gas clearance could be a safe and accurate tool for quantitating gastric mucosal blood flow.


1997 ◽  
Vol 272 (6) ◽  
pp. H2716-H2725 ◽  
Author(s):  
A. R. Pries ◽  
D. Schonfeld ◽  
P. Gaehtgens ◽  
M. F. Kiani ◽  
G. R. Cokelet

Microvessels are known to exhibit irregular shapes, deviating substantially from an idealized cylindrical tube geometry. Such irregularities must be taken into account in calculating microvascular flow resistance and may add to the observation that flow resistance in living microvessels in vivo is about twice that predicted on the basis of tube flow studies in vitro. The present study was aimed at providing a comprehensive database describing the apparent diameter variability for all segments of a complete microvascular network in the rat mesentery and assessing the impact of this variability on segmental flow resistance and the pressure drop across the network. Diameters were estimated by intravital microscopy at axial intervals of 20 microns along the 546 vessel segments of a mesenteric microvessel network, resulting in 6,319 separate diameter measurements. The amplitude of diameter variations in individual vessel segments decreased from approximately 15% of the mean vessel diameter in the smallest segments (approximately 5 microns diam) to approximately 5% in the largest segments (approximately 60 microns diam). Segmental hindrance was estimated to be 10-23% higher than calculated from arithmetic mean diameter, depending on the model used to estimate the hydrodynamically effective segment diameter. The overall pressure drop across the network calculated using a mathematical flow simulation was increased by 7-13.5%. This increase in flow resistance can explain approximately 10% of the observed discrepancy between flow resistance in vivo and in vitro.


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