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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↗
PubMed2001

Lack of hypercapnic increase in cerebral blood flow at high blood viscosity in conscious blood-exchanged rats.

BACKGROUND: The hypothesis of a compensatory dilation of cerebral vessels to maintain cerebral blood flow at a high blood viscosity was tested during hypercapnia in the study after replacement of blood by hemoglobin solutions of defined viscosities. If compensatory vasodilation exists at normocapnia at a high blood viscosity, vasodilatory mechanisms may be exhausted when hypercapnia is added, resulting in a lack of increase in cerebral blood flow at hypercapnia. METHODS: In conscious rats, blood was replaced by ultrapurified cross-linked hemoglobin solutions that had defined and shear rate-independent low or high viscosities (low- and high-viscosity groups). Blood viscosity differed threefold between both groups (1.2 vs. 3.6 mP x s). Thereafter, rats inhaled either a normal or an increased concentration of carbon dioxide in air. Cerebral blood flow was determined by the iodo[14C]antipyrine method. RESULTS: During normocapnia, global and local cerebral blood flows did not differ between both groups. With increasing degrees of hypercapnia, global and local cerebral blood flows were gradually elevated in the low-viscosity group (2.8 ml x mmHg(-1) CO2 x 100 g(-1) x min(-1)), whereas they remained unchanged in the high-viscosity group. CONCLUSIONS: Changes in blood viscosity do not result in changes of cerebral blood flow as long as cerebral vessels can compensate for these changes by vasodilation or vasoconstriction. However, such vascular compensatory adjustments may be exhausted in their response to further pathophysiologic conditions in blood vessels that have already been dilated or constricted as a result of changes in blood viscosity.

Animals↗
PubMed1988

Maternal blood viscosity and uteroplacental blood flow velocity waveforms in normal and complicated pregnancies.

According to the Poiseuille-Hagen law, viscosity influences flow resistance. A possible effect of blood viscosity upon the resistance index of the uteroplacental circulation as measured by continuous wave Doppler ultrasound was investigated in 50 pregnant women. It was found that blood viscosity variables explained only about 10% of the variation in the resistance index in all patients, which was not statistically significant. It is suggested, therefore, that the vascular contribution to flow resistance may be more important.

Blood Flow Velocity↗
PubMed1987

The effects of experimental hypo- and hyperthyroidism on blood viscosity and other blood parameters in the rat.

Three groups of male Sprague Dawley rats received methimazole without or with Na-thyroxine in drinking water (3 and 0.33 mg T4/l, respectively) to induce characteristic alterations of their thyroid status (hypothyroid, hyperthyroid, euthyroid). A fourth group served as an untreated control without any additive to the drinking water. With respect to the different thyroid status, the following changes in the blood parameters were found: increasing plasma-T3-levels caused a reduction in plasma viscosity, in total plasma protein and in alpha 1-globulin, but an increase in hematocrit, whole blood viscosity, the number of erythrocytes and leukocytes, alpha 2-globulin and beta-globulin. It was concluded that the increase in the plasma viscosity in the hypothyroid status is mainly due to an alteration of the plasma protein pattern, and that the increase in whole blood viscosity in the hyperthyroid rat is a consequence of increased hematocrit.

Animals↗
PubMed1981

Effects of increased plasma viscosity and red blood cell aggregation on blood viscosity in vivo.

The effects of increased plasma viscosity and induced red blood cell (RBC) aggregation on apparent viscosity of blood in vivo in the skeletal muscle of the dog were studied. Apparent viscosity in vivo was determined in the isolated and vasodilated calf muscles of one hindlimb by comparing pressure-flow relationships for RBC suspensions with pressure-flow relationships for a Newtonian solution of known viscosity. RBC suspensions of increased plasma viscosity with and without RBC aggregation were obtained by substituting plasma with isoviscous solutions of high- and low-molecular-weight dextran in saline. Hematocrits of the suspensions were adjusted to either 45 or 60%. The viscosities of the suspensions in vitro were determined in a Wells-Brookfield viscometer. Apparent viscosity of blood in vivo was found to be mainly dependent on the viscosity of plasma. RBC aggregation had no significant influence on the viscosity in vivo.

Animals↗
PubMedDate not supplied

[Dynamic blood viscosity in selected respiratory system diseases].

The dynamic viscosity of blood was examined in 90 persons with different pulmonary diseases ill and in 56 with a normal state of health. Age was found not to have any effect on blood viscosity both in the male and female members of the control group, whereas in women aged below 40 blood viscosity was lower from that in men both before and after 40. Blood viscosity in women after 40 did not differ from blood viscosity in men, which may be explained by the effect of hormonal factors on blood viscosity in women. In the group of ill subjects, blood viscosity values were found to be increased to various degree; the highest values of that parameter were found in persons with lungs cancer. These values depended on blood protein disturbances found in that group, especially on the high concentration in blood of fibrinogen and gamma, alfa 2 and alfa 1 globulins.

Adult↗
PubMed2001

Influence of D- and L-glucose on erythrocytes and blood viscosity.

BACKGROUND: Elevated blood glucose levels are associated with substantial morbidity and mortality. The pathomechanism behind it is not well understood. The aim of the present study was to investigate the effect of glucose on blood rheology. MATERIALS AND METHODS: Blood from healthy volunteers was incubated with various concentrations of D- and L-glucose for 1 h at 37 degrees C. Whole blood viscosity at haematocrit 45% was measured at high and low shear rate (94.5 and 0.1 s(-1)). Erythrocyte shape and volume were assessed. Haemoglobin solutions were incubated with D-glucose for up to 96 h and the viscosity was measured. RESULTS: D-glucose dissolved in H2O and diluted with isotonic NaCl, added to whole blood (additional D-glucose concentrations 0-80 mM), led to a red cell swelling and an increase in blood viscosity at low shear rate (0.1 s(-1)). This process was reversible upon removal of D-glucose. L-glucose, which is not transported into the red cell by the D-glucose-specific transport protein GLUT-1, had no effect. When D-glucose was dissolved and diluted in autologous plasma, haematocrit and viscosity remained unaffected, but L-glucose decreased both values. Incubation of a haemoglobin solution with D-glucose at 37 degrees C led to a time-dependent increase in glycosylated haemoglobin (HbA1C) up to 8%, but left the viscosity unchanged. CONCLUSION: Blood glucose tested in a wide range of concentrations did not affect blood viscosity and morphological or biophysical properties of erythrocytes.

Blood Viscosity↗
PubMed1981

Blood viscosity after splenectomy.

Blood viscosity and its contributory factors--namely, plasma viscosity, fibrinogen concentration, packed cell volume, red-cell deformability, and platelet count--were measured in 20 asymptomatic patients after splenectomy and compared with those in controls. Whole-blood viscosity was significantly increased after splenectomy and was associated with increased platelet count and, more importantly, decreased red-cell deformability. Blood viscosity was measured in six patients before and after splenectomy and in each an increase in viscosity occurred that did not occur in patients who underwent laparotomy without splenectomy. these findings suggest that the inclusions and protein complexes within the red cell that are normally removed by the spleen decrease red-cell deformability and lead to an increase in blood viscosity. This may account for the observed increase in deaths from ischaemic heart disease many years after splenectomy.

Adolescent↗
PubMed1992

Blood viscosity in tube flow: dependence on diameter and hematocrit.

Since the original publications by Martini et al. (Dtsch. Arch. Klin. Med. 169: 212-222, 1930) and Fahraeus and Lindqvist (Am. J. Physiol. 96: 562-568, 1931), it has been known that the relative apparent viscosity of blood in tube flow depends on tube diameter. Quantitative descriptions of this effect and of the dependence of blood viscosity on hematocrit in the different diameter tubes are required for the development of hydrodynamic models of blood flow through the microcirculation. The present study provides a comprehensive data base for the description of relative apparent blood viscosity as a function of tube diameter and hematocrit. Data available from the literature are compiled, and new experimental data obtained in a capillary viscometer are presented. The combined data base comprises measurements at high shear rates (u > or = 50 s-1) in tubes with diameters ranging from 3.3 to 1,978 microns at hematocrits of up to 0.9. If corrected for differences in suspending medium viscosity and temperature, the data show remarkable agreement. Empirical fitting equations predicting relative apparent blood viscosity from tube diameter and hematocrit are presented. A pronounced change in the hematocrit dependence of relative viscosity is observed in a range of tube diameters in which viscosity is minimal. While a linear hematocrit-viscosity relationship is found in tubes of < or = 6 microns, an overproportional increase of viscosity with hematocrit prevails in tubes of > or = 9 microns. This is interpreted to reflect the hematocrit-dependent transition from single- to multifile arrangement of cells in flow.

Animals↗
PubMed1996

Decreased blood viscosity and serum levels of erythropoietin after anti-hypertensive treatment with amlodipine or metoprolol: results of a cross-over study.

The increased viscosity of blood of hypertensive patients can be assumed to be a risk factor for the development of cardiovascular diseases. The aim of the present study was to elucidate whether anti-hypertensive treatment has any impact on blood rheology. Twenty patients with previously untreated hypertension who consecutively attended our outpatient hypertension clinic were included in this prospective, open, cross-over study. The patients were randomly selected to treatment with amlodipine or metoprolol. The anti-hypertensive therapy was switched after 4 months. Haemorheological and haemodynamic variables were measured with rotational viscometry and impedance cardiography, respectively. Fifteen and 16 patients could be evaluated after amlodipine or metoprolol treatment respectively. The mean blood pressure (BP) decreased from 159 +/- 22/105 +/- 7 to 139 +/- 21/91 +/- 6 mm Hg on amlodipine and from 162 +/- 22/104 +/- 5 to 145 +/- 24/90 +/- 8 mm Hg on metoprolol therapy. After amlodipine treatment, the total peripheral resistance index decreased whereas metoprolol treatment was accompanied by a decrease in the cardiac index. Decreases in whole blood viscosity, haematocrit and serum erythropoietin were found after amlodipine as well as metoprolol treatment. After amlodipine the plasma viscosity decreased and the erythrocyte deformability increased in the majority of patients. Plasma fibrinogen decreased after metoprolol treatment. Despite the differences in haemodynamic mechanisms underlying the decrease in BP, amlodipine and metoprolol exert beneficial effects on blood viscosity. Haemodilution and a decrease in serum erythropoietin may be factors underlying this decrease in blood viscosity.

Adult↗