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PubMed2005

Domain shape relaxation and local viscosity in stratifying foam films.

We studied the dynamics of two different types of domain shape relaxation in a stratifying foam film composed of an anionic polymer and cationic surfactant. Those films thin in stepwise fashion: circular domains of lower film thickness are formed, expand and coalesce until they cover the whole film surface. We found that the shape relaxation of coalescing domains is governed only by 2D dissipation, and the measurement of the time scales allows to determine the ratio between the driving force (line tension) and local film viscosity. Further, we analyzed the withdrawal of stripes and modeled it by a moving disc pulled by an external force. Here, 3D dissipation can not be neglected (Stokes paradox) and the equilibrium velocity depends logarithmically on the viscosity of the surrounding 3D air. The evaluation of both kinds of relaxation events yields the orders of magnitude of film viscosity and line tension. For the investigated system we found that the film viscosity is at least 30 times larger than the bulk viscosity, which can be explained by the local molecular ordering and strong interactions with film surfaces.

Anions↗
PubMed1985

Canine gastric emptying of fiber meals: influence of meal viscosity and antroduodenal motility.

Dietary fibers such as psyllium and guar gum have been shown to delay the gastric emptying of liquids and solids, presumably due to an increase in meal viscosity. For liquid test meals containing fats, delayed gastric emptying is associated with a reversal of the usual antral-to-duodenal contractile gradient. The present studies were performed to determine whether the gastric emptying of increasingly viscous psyllium and guar gum meals was associated with antroduodenal motility changes. Dogs were surgically fitted with mid-duodenal cannulas for the measurement of gastric emptying. Strain-gauge force transducers were used to monitor antral and duodenal contractile responses to the test meals. Low-viscosity fiber meals emptied from the stomach rapidly (E 1/2 approximately 10 min) compared with the high-viscosity meals (E 1/2 approximately 40 min). None of the test meals stimulated antral or duodenal motility despite differences in gastric emptying time. Other motor parameters such as the time of reappearance and the duration of the burst interval were also unchanged. We conclude a) as test meals' fiber content and viscosity increase, gastric emptying is slowed; and b) viscosity-related delays in gastric emptying are not due to an effect on postprandial antroduodenal motility.

Animals↗
PubMed1988

Effects of alterations in bolus viscosity on esophageal peristalsis in humans.

The effect of increased bolus viscosity on esophageal peristaltic function was studied in six healthy volunteer subjects. Intraluminal pressure events were measured with an infused catheter system and lower esophageal sphincter pressure was monitored continuously with a Dent sleeve. Boluses with viscosities of 2.5, 8.7, 48, and 860 centipoise (cP) were compared with a water bolus. Increasing bolus viscosity to 48 and 860 cP elicited a slowing of wave velocity, an increase in wave duration, and a prolongation of lower esophageal sphincter relaxation. The initial change noted at lower viscosities was an increased duration of contraction wave. Maximal changes were noted at the 48 cP bolus. In conclusion, increased bolus viscosity significantly alters human esophageal peristalsis. These changes may be mediated by esophageal stretch reflexes or by the intrinsic properties of the esophageal musculature or both.

Adult↗
PubMed2005

Microvascular blood viscosity in vivo and the endothelial surface layer.

The apparent viscosity of blood in glass tubes declines with decreasing diameter (Fåhraeus-Lindqvist effect) and exhibits a distinctive minimum at 6-7 microm. 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 approximately 0.8-1 microm for 10- to 40-microm-diameter vessels and declined strongly for smaller diameters, with an additional hematocrit-dependent impact on flow resistance exhibiting a maximum for approximately 10-microm-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.

Animals↗
PubMed1998

Plasma viscosity regulates capillary perfusion during extreme hemodilution in hamster skinfold model.

Effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation was investigated in the awake hamster skinfold model. Two isovolemic hemodilution steps were performed with 6% Dextran 70 [molecular weight (MW) = 70,000] until systemic hematocrit (Hct) was reduced by 65%. A third step reduced Hct by 75% and was performed with the same solution [low viscosity (LV)] or a high-molecular-weight 6% Dextran 500 solution [MW = 500, 000, high viscosity (HV)]. Final plasma viscosities were 1.4 and 2.2 cP (baseline of 1.2 cP). Hct was reduced to 11.2 +/- 1.1% from 46.2 +/- 1.5% for LV and to 11.9 +/- 0.7% from 47.3 +/- 2.1% for HV. HV produced a greater mean arterial blood pressure than LV. Functional capillary density (FCD) was substantially higher after HV (85 +/- 12%) vs. LV (38 +/- 30%) vs. baseline (100%). PO2 levels measured with Pd-porphyrin phosphorescence microscopy were not statistically changed from baseline until after the third hemodilution step. Wall shear rate (WSR) decreased in arterioles and venules after LV and only in arterioles after HV. Wall shear stress (WSR x plasma viscosity) was substantially higher after HV vs. LV. Increased mean arterial pressure and shear stress-dependent release of endothelium-derived relaxing factor are possible mechanisms that improved arteriolar and venular blood flow and FCD after HV vs. LV exchange protocols.

Animals↗
PubMed1985

Blood viscosity responses to maximal exercise in endurance-trained and sedentary female subjects.

To assess whether the rheological properties of blood might be altered by exercise, we measured whole blood viscosity, plasma viscosity, and its components in healthy female subjects before, immediately after, and 1 h after maximal upright exercise using the Bruce graded exercise protocol. Forty-seven female subjects (15 sedentary, 14 who ran 5-15 miles/wk, and 18 who ran greater than 50 miles/wk), ages 18-43 yr, were evaluated. Whole blood viscosity, measured with a cone and plate viscometer, increased an average of 12.6% with exercise. The increase was greater than can be attributed to the observed 8.9% increase in hematocrit alone due to a coincident increase in plasma protein concentration. However, plasma viscosity did not rise to the degree expected, likely due to a disproportionate observed loss of fibrinogen from the protein pool. These changes were independent of conditioning level or aerobic capacity. In this cross-sectional study, there appears to be no adaptive adjustment in females to physical conditioning that results in changes in blood viscosity.

Adult↗
PubMed1985

Effects of hemodilution on skeletal muscle blood flow and blood viscosity in vivo after splanchnic stasis.

Pressure-flow relationships and apparent viscosity in vivo were determined in the skeletal muscle of the dog in experimental shock induced by splanchnic venous stasis and after subsequent hemodilution with low molecular weight dextran. The calf muscles of one hind limb were surgically isolated and pressure-flow curves constructed for blood and a cell-free reference solution during vasodilation. The apparent viscosity in vivo was determined by comparing the flow values for blood and the reference solution at identical perfusion pressures. A shock state with hypotension and hemoconcentration was induced by laparotomy and splanchnic venous stasis. Hemodilution was subsequently produced by low molecular weight dextran. After splanchnic stasis, skeletal muscle blood flow decreased and viscosity in vivo increased disproportionately in relation to the increase in hematocrit. Hemodilution could reverse the flow and viscosity changes induced during the shock period. It is concluded that a shock state associated with hemoconcentration results in flow stagnation in the skeletal muscle with increased in vivo viscosity and that the changes can be reversed by hemodilution.

Animals↗
PubMed1975

Blood viscosity factors and occlusive arterial disease in renal transplant recipients.

29 cadaveric renal transplant recipients were assessed clinically for evidence of occlusive arterial disease prior to undergoing blood viscosity studies. Nineteen patients had manifest arterial disease (myocardial infarction, cerebral thrombosis, angina, intermittent claudication, absent peripheral pulses), while ten were free from vascular complications. Patients with arterial disease showed significant elevations of plasma viscosity (p less than 0.005), aggregation of red cells measured both at 37 and 20 degrees C (p less than 0.05), fibrinogen (p less than 0.005), serum triglyceride (p less than 0.01), serum cholesterol (p less than 0.01), erythrocyte sedimentation rate (p less than 0.02), and a significant reduction in the albumin/fibrinogen ratio (p less than 0.005) when compared with those free of disease. Two patients with no apparent vascular disease when investigated were found to have distinctly abnormal blood viscosity factors, and one subsequently developed retinal arterial thrombosis while the other suffered serious damage of the graft within 3 months of viscosity study. When all patients were considered together, significant correlations were found between viscosity of artificial thrombi or aggregation of red cells and fibrinogen level (both p less than 0.05), and serum triglyceride level (both p less than 0.05); and between rigidity of red cells and the parathyroid hormone level (p less than 0.01).

Adult↗
PubMed1980

Effect of hematocrit on the blood viscosity of patients with chronic respiratory failure and secondary polycythemia.

The blood of patients with chronic global respiratory failure and polycythemia exhibits higher viscosity than that of normal subjects. Plasma changes have been excluded as causal factors. The viscosity of whole blood, plasma and blood after correction of hematocrit (Ht; 45%) with autologous plasma, has been determined. The results indicate that in such patients the increase in Ht is not the most important factor affecting the rheological properties (increased viscosity) of blood. A high Ht value may be only pat of the mechanism that increases the blood viscosity of patients with chronic obstructive pulmonary disease. There is evidence that other factors are responsible for increased blood viscosity in chronic respiratory failure.

Blood Viscosity↗
PubMed1992

Effects of tung oil on salivary viscosity and extent and incidence of dental caries in rats.

Increased salivary viscosity may be associated with an increase in dental caries. In order to examine this relationship, the caries level in rats was monitored following gastric intubation with tung oil which has been shown to significantly increase salivary viscosity. Tung oil intubation over an 8-week period significantly increased the salivary viscosity in rats as compared with deoinized water and corn oil intubation. The total number of carious lesions was significantly increased (p less than 0.05) in the tung oil intubated rats as compared with the two other groups. This increase in carious lesions was primarily associated with the smooth surfaces of the teeth. There was also a significant increase (p less than 0.05) in the extent of enamel and dentin involvement of the tung oil intubated rats as compared with the other two groups. Histologic examination of the submandibular glands revealed an increase in the amount of glycoprotein material in the convoluted granular tubules of the tung oil intubated rats as compared with the deionized water and corn oil intubated animals. Collectively, these results suggest that tung oil intubation is correlated with both increased salivary viscosity and increased smooth-surface dental caries, suggesting that the viscosity may be related to dental caries progression.

Animals↗
PubMed1993

Blood viscosity, fibrinogen, and activation of coagulation and leukocytes in peripheral arterial disease and the normal population in the Edinburgh Artery Study.

BACKGROUND: Increased blood and plasma viscosity, hematocrit, fibrinogen, and activation of coagulation and leukocytes have been reported in patients with claudication; however, their associations with symptomatic and asymptomatic peripheral arterial disease have not been reported in an epidemiological study. METHODS AND RESULTS: Blood and plasma viscosity, hematocrit, fibrinogen, urinary fibrinopeptide A, plasma leukocyte elastase, and uric acid were measured in a random sample of 1,581 men and women aged 55-74 years in Edinburgh, Scotland, and related to peripheral arterial stenosis (ankle-brachial systolic pressure index, ABPI) and to lower limb ischemia (intermittent claudication and reactive hyperemia test). Each variable (except fibrinopeptide A) was significantly related to prevalent symptomatic and asymptomatic peripheral arterial disease. On multivariate analysis, blood viscosity (p < 0.05) and fibrinogen (p < 0.01) were independently associated with peripheral arterial narrowing (ABPI); a positive interaction was found between fibrinogen and smoking in the association with ABPI. Plasma viscosity was associated with claudication in the presence of a given degree of arterial narrowing (odds ratio of claudication in top quintile compared with bottom quintile of plasma viscosity, 3.35; 95% CI, 1.32, 8.51). Leukocyte elastase and uric acid were each associated with reactive hyperemia independently of arterial narrowing (p < 0.01). CONCLUSIONS: Blood rheological factors and leukocyte activation as well as arterial narrowing are associated with lower limb ischemia in the general population and may be implicated in its pathogenesis.

Aged↗
PubMed2004

Hemodilution with stroma-free [correction of stoma-free] hemoglobin at physiologically maintained viscosity delays the onset of vasoconstriction.

Solutions of modified cell-free hemoglobin, prepared from outdated red blood cells, have been developed during the past decade to circumvent the increasing need for allogeneic blood. Despite improvements in the safety and efficacy of these solutions, undesirable effects such as an increase in vascular tone leading to hypertension have not been fully resolved, which might hinder their clinical usefulness. To discriminate between the pharmacological and rheological effects of cell-free hemoglobin, we compared the effects of blood/cell-free hemoglobin mixtures of high versus low viscosity on hemodynamics and vascular hindrance, an index of vascular tone, which was normalized for blood viscosity. Anesthetized rats were subjected to 50% exchange transfusion with (1) high-viscosity solutions: whole blood (n=5) or red blood cells mixed with cell-free hemoglobin (Hb-Hv group, n=5); (2) low-viscosity solutions: cell-free hemoglobin (Hb-Lv group, n=5) or human albumin (n=5). Two hours after hemodilution, vascular hindrance remained unchanged in animals transfused with whole blood and albumin. Hb-Lv induced an immediate and sustained increase in vascular hindrance (208%). Conversely, in Hb-Hv animals, the vascular hindrance increase was delayed and smaller (27% to 147%), whereas peripheral resistance increased gradually (94% after 2 hours). Our results demonstrate the beneficial effects of cell-free hemoglobin in the presence of the animals' own red blood cells in maintaining physiological viscosity and limiting vasoconstriction because of the pharmacological properties of cell-free hemoglobin.

Animals↗
PubMed1981

Blood flow and in vivo apparent viscosity in working and non-working skeletal muscle of the dog after high and low molecular weight dextran.

We studied the effect of high and low molecular weight dextran on blood flow and in vivo apparent viscosity in the vasodilated vascular bed of working and non-working skeletal muscle. In 12 mongrel dogs, the calf muscle of one hindlimb was isolated. Vasodilation was induced either by sciatic stimulation setting the muscle at rhythmic work or by intraarterial infusion of papaverine. Blood flow was measured electromagnetically at different perfusion pressures. In vivo apparent viscosity was calculated by comparing pressure-flow relationship for blood and a reference solution. Viscosity in vitro was determined in a cone-plate viscometer. A hyperviscous state was induced by intravenous infusion of high molecular weight dextran (HMWD). Hemodilution subsequently was produced by administration of low molecular weight dextran (LMWD). After HMWD, blood flow decreased to 30% of control values in the non-working group and to 45% of control values in the working group. After subsequent infusion of LMWD, blood flow returned to 60% of control values in the non-working group and to 70% of control values in the working group. In vivo apparent viscosity increased to values 250% above control in the non-working group and to 120% above control in the working group following HMWD. After subsequent infusion of LMWD in vivo, apparent viscosity decreased, but remained at values 65% above control in the non-working group and 45% above control in the working group. Thus, the flow impairment induced by HMWD was less pronounced in the working muscle, indicating a flow-preserving effect of rhythmic muscle contractions in this state of disturbed blood rheology. In contrast, the flow-improving effect of LMWD by hemodilution was more pronounced in the non-working muscle.

Animals↗
PubMed1993

Role of shear stress and endothelial prostaglandins in flow- and viscosity-induced dilation of arterioles in vitro.

We have studied the effect of changes in shear stress on diameter of isolated arterioles of rat cremaster muscle. The steady-state active diameter of arterioles at a constant perfusion pressure (60 mm Hg) was 80 +/- 1.2 microns. The vessels' passive diameter (Ca(2+)-free solution) was 156 +/- 1.8 microns. Changes in shear stress were induced either by an increase in flow (velocity) or by an increase in viscosity of the perfusion solution. At a constant perfusion pressure, the stepwise increase in perfusion flow (0-80 microliters/min in 10-microliters/min steps) elicited, with a delay of approximately 20 seconds, a gradual increase in diameter up to 46%. At a constant 20-microliters/min flow rate, increases in viscosity of the perfusate (2%, 4%, and 6% dextran [molecular weight, 77,800]) caused a gradual vasodilation up to 22%. Varying flow and viscosity of the perfusate simultaneously resulted in an upward shift of the flow-diameter curve. Both flow- and viscosity-induced dilations were eliminated by the removal of the endothelium of arterioles (by air) or were inhibited by indomethacin (10(-5) M). The efficacy and specificity of these inhibitory treatments were assessed with vasoactive agents whose action, with regard to endothelial mediation, has been determined previously. The arteriolar dilation maintained calculated wall shear stress close to control values during increases in flow and/or viscosity of the perfusate, but when the dilation was inhibited by removal of the endothelium or by indomethacin, wall shear stress increased significantly in a cumulative manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity.

BACKGROUND: During maximal hyperemia, capillaries provide the greatest resistance to flow. A major determinant of capillary resistance is viscosity. We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion. METHODS AND RESULTS: Maximal hyperemia was induced in 9 dogs using adenosine. Serum triglyceride levels were increased by incremental doses of Intralipid. A good correlation was noted between serum triglyceride levels and blood viscosity (r=0.82). Neither total coronary blood volume nor myocardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion. Myocardial vascular resistance (MVR) increased with increasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64). The decrease in hyperemic MBF was associated with a decrease in blood velocity (r=-0.56). These findings were confirmed with direct intravital microscopic observations in the mice cremaster muscle. CONCLUSIONS: Increasing lipid levels in a fully dilated normal coronary bed causes no change in large or small vessel dimensions. Instead, the increase in blood viscosity causes capillary resistance to rise, which attenuates hyperemic CBF. Therefore, the abnormal CBF reserve associated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function.

Adenosine↗
PubMed2005

Gel strength and solution viscosity of temperature-sensitive, in-situ-gelling polymers for endovascular embolization.

The goal of this work was to investigate the relationship of the gel strength and stiffness (at 37 degrees C) to solution viscosity (at 25 degrees C) in poly(N-isopropylacrylamide-co-acrylic acid) solutions with regard to acid content, molecular weight and solution concentration. It was hypothesized that the gel strength could be maximized while minimizing the increase in solution viscosity. If so, there would be motivation to investigate these materials for arteriovenous malformation embolization. The co-polymers were synthesized with 0-2 mol% content of acrylic acid (AAc) in benzene, dioxane, THF, 50:50 benzene/dioxane, or 50:50 dioxane/THF to obtain polymers of different molecular weight. The polymers were characterized for molecular weight by GPC/light scattering, for acrylic acid content by acid titration, for lower critical solution temperature by differential scanning calorimetry, and for solution viscosity (at 25 degrees C) and gel strength (at 37 degrees C) by rheometry. Solutions of lower-molecular-weight polymers were shown to have lower viscosities while possessing higher strengths as gels than the highest manageable concentrations of higher-molecular-weight polymers. This work demonstrates that the mechanical properties of poly(N-isopropylacrylamide-co-acrylic acid) can be increased while minimizing the increase in solution viscosity.

Acrylamides↗
PubMed2002

Transport properties of nanosystems: viscosity of nanofluids confined in slit nanopores.

A fundamental nonequilibrium statistical mechanical approach due to Pozhar and Gubbins (PG) is used to study the Poiseuille flow and momentum transport in 20 model nanofluids confined in slit pores several molecular diameters in width. A simplified version of a general expression for the PG theoretical viscosity is applied to calculate the localized viscosity of the nanofluids in terms of the equilibrium structure factors (density and correlation functions) of nanosystems. These structure factors are calculated by means of the equilibrium molecular dynamics simulations. The localized theoretical viscosity so obtained is used further to calculate the theoretical pore-average viscosity of the nanosystems, and the latter is successfully compared with that extracted from nonequilibrium molecular dynamics simulation data. A simple correlation between the pore-average velocity, viscosity, nanofluid density, and the pore width for nanosystems of moderate density has been developed and recommended for applications in engineering.

Computer Simulation↗
PubMedDate not supplied

Molecular viscosity in the normal left coronary arterial tree. Is it related to atherosclerosis?

The purpose of this study is to elucidate, probably for the first time, the distribution of molecular viscosity in the entire left coronary artery (LCA) tree. The governing mass, momentum, and energy flow equations were solved by using a previously validated 3-dimensional numerical (finite-element analysis) code. High-molecular-viscosity regions occur at bifurcations in regions opposite the flow dividers, which are anatomic sites predisposed for atherosclerotic development. Furthermore, high-molecular-viscosity values appear in the proximal regions of the LCA tree, where atherosclerosis frequently occurs. The effect of blood flow resistance, due to increased blood viscosity, gives rise to increased contact time between the atherogenic particles of the blood and the endothelium, probably promoting atherosclerosis. Observations suggest that, whole viscosity distribution within the coronary artery tree may represent a risk factor for the resulting atherosclerosis. This distribution can become a possible tool for the location of atherosclerotic lesions.

Blood Flow Velocity↗