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At least 883 records · Page 49Linked to original sources
PubMed2006

Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity.

Responses to exchange transfusion with red blood cells (RBCs) containing methemoglobin (MetRBC) were studied in an acute isovolemic hemodiluted hamster window chamber model to determine whether oxygen content participates in the regulation of systemic and microvascular conditions during extreme hemodilution. Two isovolemic hemodilution steps were performed with 6% dextran 70 kDa (Dex70) until systemic hematocrit (Hct) was reduced to 18% (Level 2). A third-step hemodilution reduced the functional Hct to 75% of baseline by using either a plasma expander (Dex70) or blood adjusted to 18% Hct with all MetRBCs. In vivo functional capillary density (FCD), microvascular perfusion, and oxygen distribution in microvascular networks were measured by noninvasive methods. Methylene blue was administered intravenously to reduce methemoglobin (rRBC), which increased oxygen content with no change in Hct or viscosity from MetRBC. Final blood viscosities after the entire protocol were 2.1 cP for Dex70 and 2.8 cP for MetRBC (baseline, 4.2 cP). MetRBC had a greater mean arterial pressure (MAP) than did Dex70. FCD was substantially higher for MetRBC [82 (SD 6) of baseline] versus Dex70 [38 (SD 10) of baseline], and reduction of methemoglobin to oxyhemoglobin did not change FCD [84% (SD 5) of baseline]. P(O2) levels measured with palladium-meso-tetra(4-carboxyphenyl)porphyrin phosphorescence were significantly changed for Dex70 and MetRBC compared with Level 2 (Hct 18%). Reduction of methemoglobin to oxyhemoglobin partially restored P(O2) to Level 2. Wall shear rate and wall shear stress decreased in arterioles and venules for Dex70 and did not change for MetRBC or rRBC. Increased MAP and shear stress-mediated factors could be the possible mechanisms that improved perfusion flow and FCD after exchange for MetRBC. Thus the fall in systemic and microvascular conditions during extreme hemodilution with low-viscosity plasma expanders seems to be, in part, from the decrease in blood viscosity independent of the reduction in oxygen content.

Anemia↗
PubMed1978

Accentuation of heart sounds in anemia: an effect of blood viscosity.

The effect of blood viscosity on the intensity of heart sounds was investigated in 25 anemic patients and 41 control subjects. Calibrated phonocardiograms showed that in anemic patients, the aortic component of the second sound was of greater amplitude (54 +/- 3 vs. 33 +/- 3 dyn/cm2) (P less than 0.001). The pulmonary component of the second sound and the first sound were also of higher amplitude in anemic patients (both P less than 0.001). The viscosity of blood of anemic patients was lower (0.029 +/- 0.001 vs. 0.045 +/- 0.001 poise) (P less than 0.001). Blood pressure was comparable among the two groups. Sound produced by closure of a normal porcine valve in an in vitro flow system also showed an accentuated sound with liquids of lower viscosity. Augmented diastolic vibrations of the closed valve, shown by high-speed motion pictures, accompanied the accentuated sound. These observations suggest that the accentuated second sound in anemic patients results from the lower blood viscosity, which reduces the damping forces that act upon the semilunar valve as it vibrates after closure. The reduced damping would allow augmented vibrations that result in an accentuated sound.

Anemia↗
PubMed1994

Effect of increased whole blood viscosity on regional blood flows in chronically hypoxemic lambs.

In chronic hypoxemia blood flow and oxygen supply to vital organs are maintained, but to nonvital organs they are decreased. We measured organ blood flows (microspheres) and whole blood viscosity in 10 chronically hypoxemic lambs, with an atrial septal defect and pulmonary stenosis, and in 8 control lambs. Vascular hindrance (resistance/viscosity) was calculated to determine to what extent the effect of increased blood viscosity on organ blood flow was compensated for by a decrease in vascular tone. Arterial oxygen saturation was decreased (68 +/- 10 vs. 91 +/- 3%, P < 0.001), and both hemoglobin concentration (145 +/- 10 vs. 109 +/- 9 g/l, P < 0.05) and blood viscosity (4.4 +/- 0.6 vs. 3.6 +/- 0.6 mPa.s, P < 0.05) were increased in hypoxemic lambs. Systemic blood flow, oxygen supply, oxygen uptake, and blood pressures were not significantly different between hypoxemic and control lambs. Myocardial and cerebral blood flow was maintained in hypoxemic lambs, whereas renal, gastrointestinal, splenic, and thyroidal blood flows were at least 30% lower. Vascular hindrance was significantly decreased in the myocardium and tended to be lower in the brain of hypoxemic lambs, but in all other organs it was similar to that in control lambs. It is concluded that blood flow is redistributed in chronic hypoxemia in lambs; myocardial and cerebral blood flow is maintained, whereas blood flow to splanchnic organs, the kidneys, and the thyroids is decreased. The decreased blood flow to organs is a consequence of the increased whole blood viscosity.

Animals↗
PubMed2006

Mechanosensitivity of mouse tracheal ciliary beat frequency: roles for Ca2+, purinergic signaling, tonicity, and viscosity.

Mechanosensitivity is hypothesized to participate in the regulation of ciliary beat frequency (CBF) in airway epithelia. To investigate this hypothesis, CBF in excised mouse trachea was monitored (microscopy image analysis) while varying mucosal shear (perfusate velocity and/or viscosity; planar flow). CBF increased within minutes of step increase to steady shear stress as small as 10(-3) Pa and decreased within minutes of shear reduction (<or=10(-4) Pa). CBF response was directional, being less with cephalad vs. caudal flow, and was reduced in trachea from mutant mice lacking P2Y2 receptors, as well as by administration of the Ca2+ chelator EGTA, the Ca2+ channel inhibitor La3+, the nucleotide phosphohydrolase apyrase, the metabolically stabilized adenosine receptor agonist 5'-(N-ethylcarboxamido)adenosine, the osmotic agent mannitol, and the viscosity modifier dextran. Brief exposure to exogenous ATP, a candidate mediator, augmented CBF response, although augmentation declined with higher ATP concentration (5.0 vs. 0.1 mM) or longer ATP exposure before shear (55 vs. 20 min). Prolonged extended exposure (45 min) to the metabolically stabilized ATP analog ATPgammaS [adenosine 5'-(3-thiotriphosphate), 0.1 mM] inhibited CBF response to shear. Furthermore, neither ATP nor ATPgammaS substantially increased CBF in the relative absence of shear. With viscosity increase or shear withdrawal apyrase evoked CBF stimulation, inhibitable by the adenosine receptor antagonist 8-(p-sulfophenyl)theophylline. Thus CBF response to shear is finely tuned, directional, La3+ sensitive, likely dependent on extracellular Ca2+ and ATP, involving P2Y2 and adenosine receptor activations, influenced by shear history, tonicity, viscosity, and metabolism/exposure of ATP, and thus reflective of a complex interplay of physical and biochemical actions.

Adenosine Triphosphate↗
PubMed1982

Measurement of gas viscosity with a Fleisch pneumotachograph.

A simple rapid method of measuring gas viscosity using a standard Fleisch pneumotachograph and a 3-liter hand-driven syringe is described. Comparison of pneumotachographic and predicted viscosity of five pure gases (CO2, N2, He, O2, and Ar), two binary mixtures (He-O2 and N2-O2), and one quaternary mixture (He-air) gave an overall coefficient of correlation of 0.987 and an accuracy of better than 1.7%. Our data show the well-known marked curvilinear relationship between viscosity and the concentration of helium in air and oxygen mixtures. These studies indicate that a Fleisch pneumotachograph can be used as a simple accurate gas viscometer to characterize gas mixtures in terms of viscosity.

Gases↗
PubMed2000

Constraints on cardiac hypertrophy imposed by myocardial viscosity.

Laplace's law constrains how thin the ventricular wall may be without experiencing excessive stress. The present study investigated constraints, imposed by myocardial viscosity (resistance to internal rearrangement), on how thick the wall may be. The ventricle was modeled as a contracting, spherical shell. The analysis demonstrated that viscosity generates stress and energy dissipation with inverse fourth- and eighth-power dependence, respectively, on distance from the cavity center. This result derives from the combination of squared dependence of viscous forces on shearing velocity gradients and the greater shear rearrangement required for inner layers of a contracting sphere. These predictions are based solely on geometry and fundamentals of viscosity and are independent of material properties, cytoskeletal structure, and internal structural forces. Calculated values of energy and force required to overcome viscosity were clearly large enough to affect the extent of thickening of the left ventricle. It is concluded that load-independent viscous resistance to contraction is an important factor in cardiac mechanics, especially of the thickened ventricles of concentric hypertrophy.

Cardiomegaly↗
PubMed1976

Exercise fitness, cardiac work and blood viscosity factors in patients and normals.

A study of 41 cardiovascular patients and normals showed significant correlations between physical fitness (as expressed by a fitness index based on work output) and high shear rate blood viscosity (p less than 0.01); between the cardiac work expressed as double product (= myocardial oxygen demand) and aggregation of red cells (p less than 0.05); between the triple term of cardiac work (fitness index divided by double product) and high shear rate blood viscosity (p less than 0.005) or aggregation of red cells (p less than 0.05), in all cases correlations being negative i.e., higher cardiac work or higher fitness being related to low blood viscosity or lower aggregation of red cells. Significant differences were found between high-fitness and low-fitness groups, the high-fitness group showing from plasma viscosity (p less than 0.0005), lower fibrinogen level (p less than 0.05), and higher albumin/fibrinogen ratio (p less than 0.01).

Adult↗
PubMed1982

Blood viscosity in experimental acute renal failure.

We measured blood viscosity in rats 24 h after induction of acute renal failure by glycerol or HgCl2 injections. The blood viscosity values of rats with acute renal failure were significantly higher than those of controls at any shear rates. The mean values of plasma fibrinogen in animals with glycerol - (302.5 +/- 35.2 mg/100 ml) or HgCl2 - (342.1 +/- 15.9 mg/100 ml) induced acute renal failure were significantly elevated compared to control levels (169.6 +/- 16.7 mg/100 ml). We believe that the increased blood viscosity in acute renal failure was primarily due to high concentration of plasma fibrinogen. The elevated blood viscosity may affect capillary microvascular circulation of glomerular capillary beds.

Acute Kidney Injury↗
PubMed1982

A hypothesis proposing increased blood viscosity as a cause of proteinuria and increased vascular permeability.

Currently accepted concepts of renal and vascular physiology are inadequate to explain the reversible increases in vascular permeability which occur during episodes of increased blood viscosity. On the basis that all basement membranes exhibit biological thixotropy, it has been suggested that basement membranes are pressure dependent. The physiological significance of increased blood viscosity lies in the associated increase in peripheral vascular resistance which develops because of altered blood rheology. In order to overcome the peripheral resistance, intravascular pressure rises, and if adequate pressures develop, plasma proteins may deform and pass through the vascular basement membrane. This is considered to be the mechanism of proteinuria. In the treatment of high blood viscosity disorders it is suggested that the immunosuppressant drug, Thiamphenicol, may be useful because of its ability to induce a reversible dose-related depression of erythropoiesis, and thereby reduce blood viscosity.

Blood Viscosity↗
PubMed1976

[Viscosity and density fluctuations of natural respiratory gases and of mixtures of helium, oxygen and nitrogen due to temperature and composition of the gas mixture (author's transl)].

For the estimation and correction of errors in the measurement of the respiratory flow with viscosity-affected respiratory flow receptors the viscosity of natural respiratory gases (N2, O2, CO2, H2O) and of the ternary system helium-oxygen-nitrogen, which is of importance in pulmonary function diagnosis, was determined. Corresponding density values were calculated. Allowance was made for such special features of spirometry as exchange of O2 for CO2 and water vapour saturation at 37 degrees C. The viscosity of the ternary system is shown in a graph. The formulae indicated have been simplified as far as this was compatible with the demands of accuracy. The fluctuations in density and viscosity of natural respiratory gases can be read directly from a table.

Carbon Dioxide↗
PubMed1986

Effect of sucralfate on the viscosity of gastric mucus and the permeability to hydrogen ion.

The effect of sucralfate on the viscosity of pig gastric mucus and on its ability to retard the diffusion of hydrogen ion was investigated. Using a cone/plate viscometer at shear rates between 1.15 and 230 s-1, it was found that preincubation of mucus with increasing concentrations of sucralfate led to a gradual enhancement of the mucus viscosity. This enhancement in viscosity was proportional to the sucralfate concentration up to 1.0 X 10(-4) M and increased about 18% for each 10-fold increment in its concentration. The permeability measurements, conducted in a specially designed two compartment chamber, revealed that addition of sucralfate to gastric mucus had a profound beneficiary effect on its ability to retard the diffusion of hydrogen ion. In the presence of 1.0 X 10(-6) M sucralfate the permeability of mucus to hydrogen ion decreased by 35%, while the 1.0 X 10(-3) M sucralfate reduced the mucus permeability by 68%. The results show that sucralfate increases the viscosity of gastric mucus and improves its ability to impede the hydrogen ion penetration.

Aluminum↗
PubMed1987

Effect of solon on gastric mucus viscosity, permeability to hydrogen ion, and susceptibility to pepsin.

The effect of a new antiulcer drug, solon (sofalcone), on gastric mucus viscosity, permeability to hydrogen ion and degradation by pepsin was investigated using an in vitro system. Preincubation of the isolated gastric mucus with solon produced a marked enhancement in mucus viscosity. This enhancement was concentration dependent and at 2.2 X 10(-1) M solon reached a value of 230%. Permeability measurements showed that 2.2 X 10(-2) M solon increased the retardation ability of mucus to hydrogen ion by 32%, while 43% increase was obtained with 2.2 X 10(-1) M solon. The drug had no effect on the viscosity and hydrogen ion retardation capacity of albumin. The results of peptic activity assay indicated that solon had an inhibitory effect on the rate of mucus and albumin proteolysis. The rate of inhibition of peptic activity was proportional to the solon concentration up to 1.0 X 10(-5) M, at which concentration the proteolysis of mucus was inhibited by 60% and that of albumin by 45%. The results obtained here under in vitro conditions suggest that solon, by inhibiting peptic erosion of the mucus layer, increasing its viscosity and enhancing the ability to impede the hydrogen ion penetration, strengthens the gastric mucosal integrity and thus could aid in ulcer healing.

Animals↗
PubMed1986

Effect of a reduction in blood viscosity on maximal myocardial oxygen delivery distal to a moderate coronary stenosis.

This study tested the hypothesis that a reduction in blood viscosity by means of isovolumetric hemodilution will permit an increase in maximal oxygen delivery to myocardium distal to a moderate coronary arterial stenosis. It is known that blood viscosity is a determinant of resistance to blood flow at both the stenotic and the arteriolar levels. Accordingly, a reduction in blood viscosity could exert a favorable influence on maximal myocardial oxygen delivery in the setting of stenosis, provided that the oxygen-carrying capacity of the blood is not compromised excessively. Closed-chest, sedated domestic swine (n = 8) were instrumented with an artificial coronary arterial stenosis that reduced vessel diameter by 64%. Measurements of hemodynamics, regional myocardial blood flow (microspheres), lactate and oxygen metabolism, and whole blood viscosity were made at control and after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Next, albumin/saline solution was given intravenously to reduce the animal's hematocrit by approximately 50%. Repeat measurements of all experimental variables were then made at a second control and again after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Myocardial blood flow (ml/min/g) distal to the stenosis increased from 1.52 +/- 0.21 (mean +/- 1 SD) to 4.10 +/- 0.86 in response to adenosine (peak dose) before hemodilution (p less than .01) and from 2.07 +/- 0.59 to 4.08 +/- 0.93 (p less than .01) after hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1998

Carotid wall viscosity increase is related to intima-media thickening in hypertensive patients.

Increases in arterial wall viscosity and intima-media thickness (IMT) were found in hypertensive patients. Because smooth muscle cells are responsible for the viscous behavior of the arterial wall and they are involved in the process of thickening of the intima-media complex, this study evaluates the relationship between carotid thickness and wall viscosity. The simultaneous and noninvasive assessment of the intima-media complex and arterial diameter waveform was performed using high-resolution ultrasonography. This technique was contrasted against sonomicrometry in sheep, showing that the waveforms obtained by both methods were similar. The common carotid arteries of 11 normotensive subjects (NTA) and 11 patients with mild to moderate essential hypertension (HTA) were measured noninvasively by using tonometry and an automatic densitometric analysis of B-mode images to obtain IMT and instantaneous pressure and diameter loops. A viscoelastic model was used to derive the wall viscosity index (eta) using the hysteresis loop elimination criteria. In NTA, eta was 2.73+/-1.66 (mm Hg x s/mm) and IMT was 0.58+/-0.08 (mm), whereas in HTA, eta was 5.91+/-2.34 (P<.025) and IMT was 0.70+/-0.12 (P<.025), respectively. When all data of eta versus IMT of NTA and HTA were pooled in a linear regression analysis, a correlation coefficient of r=.71 (P<.05) was obtained. Partial correlation between eta and IMT holding constant pressure was r=.59 (P<.05). In conclusion, wall viscosity increase was associated with a higher IMT even maintaining blood pressure fixed, suggesting that the intima-media thickening might be related to smooth muscle alterations manifested as an increase in viscous behavior.

Algorithms↗
PubMedDate not supplied

Whole blood viscosity parameters and cerebral blood flow.

This report describes the statistical relationship of several whole blood viscosity parameters and cerebral blood flow (CBF) in 53 consecutive patients and normal controls. Significant correlations were present between CBF and serum fibrinogen (P = .05), hematocrit (P less than .05), and a relationship involving both fibrinogen and hematocrit (P less than .01). We conclude that heightened whole blood viscosity does correlate with decreased cerebral blood flow in the ranges measured in our patients, that both fibrinogen and hematocrit must be taken into consideration in viscosity determinations, and that changes in viscosity may have an important effect on CBF in regions of low flow.

Adult↗
PubMedDate not supplied

Fibrinogen, blood viscosity, and cerebral ischemia.

This study examines the effect of fibrinogen and consequent blood viscosity reduction on cerebral blood flow and cellular injury following severe cerebral ischemia for 30 minutes in 78 Wistar rats. In half of these rats 10 to 15 cc's of blood was removed and replaced with a mixture of 5% albumin and autologous red blood cells maintaining a constant hematocrit but resulting in a 30% decrease in fibrinogen and corresponding reduction in viscosity. Fibrinogen reduction in a slight increase in baseline CBF and the elimination of post-ischemic hyperemia at 24 hours. Both study and control animals showed a similar decrease in CBF at 30 minutes and 2 hours. There was no significant difference in the severity of ischemic cellular change between the fibrinogen reduction group and controls, although there was a significant inverse relationship between the amount of viscosity change and severity of cellular injury within the treatment group. Fibrinogen reduction alone cannot significantly ameliorate ischemic injury in this model. Viscosity reduction therapy should include reduction of hematocrit and alteration of red cell deformability.

Animals↗
PubMed1987

Viscosity and spinability of nasal secretions induced by different provocation tests.

In the human nose, secretions can be experimentally induced in vivo and sampled by simple means for biophysical and biochemical analyses. It was the aim of the present study to compare viscosity and spinability of nasal secretions induced by different types of stimulation, i.e., provocation with methacholine, histamine, and allergen. The results showed considerable inhomogeneity of the samples with regard to both parameters, increased viscosity with time after consecutive allergen provocations (p less than 0.01), lower viscosity of methacholine- than of histamine- and allergen-induced secretions (p less than 0.05), comparable spinability of the 3 types of secretions, and a positive correlation between viscosity and spinability (p less than 0.01).

Adolescent↗
PubMed1978

Chemical markers of mucous and serum glycoproteins and their relation to viscosity in mucoid and purulent sputum from various hypersecretory diseases.

Mucus and serum are always present in sputum. The concentrations of their markers were measured in mucoid and purulent sputum from patients with chronic bronchitis, asthma, cystic fibrosis, or bronchiectasis. Differences in the concentrations of both mucous and serum glycoproteins were greater among different macroscopic types of sputum than among diseases for the same macroscopic type. Comparison between diseases showed that sputum from patients with asthma had the widest variation in concentrations of markers of mucous glycoprotein and dry macromolecular weight. When the asthma group was further analyzed, it became apparent that patients with extrinsic asthma without chronic bronchitis represented a homogeneous group, whereas those with intrinsic asthma, with or without chronic bronchitis, were responsible for the wide variation. The concentrations of markers of mucous and serum glycoproteins in a sputum sample were correlated with the apparent viscosity of the sputum to establish the relative contribution of the glycoproteins to the viscosity of sputum. In mucoid sputum, the mucous glycoprotein was most important in determining the viscosity, whereas when in infected sputum, both mucous and serum components contributed to the viscosity.

Asthma↗