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[Clinical and statistical considerations on the relation between hematocrit value and blood viscosity].

Blood viscosity at various speed gradients was determined in 186 patients, a range of 245 haematocrit readings varying between 12 and 72 being examined. Statistical analysis of the results revealed a direct proportionality relationship between the two parameters, with viscosity expressed in logarithms. The regression lines accentuate their slope as the speed gradient falls. When determined at high speed gradients, blood viscosity can quintuplicate its value by varying the haematocrit from 10 to 70, while it can increase fully ten times at low speed gradients with the same haematocrit reading variations. Using blood from the same subject, resuspended at different haematocrits, viscosity values were obtained along the lines of regression up to haematocrits of about 70; for higher readings, viscosity data lie above these lines to a greater extent the higher is the speed gradient. Emphasis is laid on the great importance of the haematocrit reading from the rheological viewpoint and the significant clinical deductions that can be made.

Adult

Peripheral circulation in the newborn: interaction of peripheral blood flow, blood pressure, blood volume, and blood viscosity.

Peripheral blood flow and systolic blood pressure (strain-gauge plethysmograph), blood volume (Evans blue) and whole blood viscosity (cone-plate viscometer) have been measured in 66 premature and full-term infants 6 to 144h of age. Blood flow and blood volume were moderately decreased in the infants with respiratory distress. Highly significant (P less than 0.001) correlations were found between blood flow and blood volume (r = 0.77), blood pressure and blood volume (r = 0.50), peripheral resistance and blood volume (r = -0.44), blood flow and blood pressure (r = 0.50), blood flow and peripheral resistance (r = -0.67), peripheral resistance and blood viscosity (r = 0.45), and blood viscosity and haematocrit (r = 0.86). There was no correlation between peripheral blood flow and blood viscosity. However, at given blood volume, peripheral blood flow decreased with increasing blood viscosity. These results indicate that in newborn infants peripheral blood flow, blood pressure and peripheral resistance are influenced by blood volume, but also depend on blood viscosity.

Blood Circulation

Subcutaneous ancrod therapy in peripheral arterial disease: improvement in blood viscosity and nutritional blood flow.

Nine patients with extensive peripheral arterial disease were treated with subcutaneous injections of ancrod (Arvin) for 10 to 21 days. Reduction in plasma fibrinogen was associated with a sustained reduction in plasma and blood viscosity, and a sustained increase in nutritional skin blood flow, measured by a Xenon-133 clearance technique (P less than 0.001). These findings may be relevant to the therapeutic effect of ancrod in ischemic rest pain.

Adult

Raynaud's disease: reduced hand blood flows with normal blood viscosity.

Hand blood flows and the blood and plasma viscosities were measured in patients with Raynaud's disease in an attempt to identify the mechanism of the episodic vascular insufficiency. Using venous occlusion plethysmography the following observations were made: (1) the hand blood flows were significantly less than in normals at 32 degrees, 27 degrees and 20 degrees C; (2) the percentage decrease in flow with cooling was greater in normals and (3) cooling of one hand from 32 degrees to 27 degrees C caused an abnormal decrease in flow through the contralateral hand. Using a rotational viscometer the blood and plasma viscosities were found to be normal at both high and low shear rates. The percentage increase in the blood viscosity with cooling from 35 degrees to 25 degrees was also normal. These studies demonstrate an increased constrictive response of the cutaneous vasculature of the hand to both local and reflex stimulation, and exclude a rheological abnormality, under conditions similar to those of the present study.

Adolescent

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

Hemodynamic functions and blood viscosity in surface hypothermia.

Hemodynamic functions and blood viscosity changes in hypothermia (core approximately 25 degrees C) were studied in 14 pentobarbital-anesthetized dogs subjected to surface cooling. The viscosity of blood (eta B) increased progressively to 173% of that at 37 degrees C when body temperature was lowered to 25 degrees C. The increase in blood viscosity was caused by: a) the direct effect of low temperature on plasma viscosity, b) hemoconcentration as a result of plasma loss, and c) the low-flow (low-shear) state induced by hypothermia. A larger portion of the increased viscosity was caused by the low-flow state in hypothermia. The systemic flow resistance (SFR) increased to 271% of control, and this was attributable about equally to the increases in blood viscosity and systemic vascular hindrance (SFR/eta B). Similarly, the viscosity of blood contributed significantly to raising the pulmonary flow resistance. The relative constancy of mixed venous O2 saturation suggests that the cardiac output at low body temperature is generally adequate to meet the metabolic needs.

Animals

Effects of long-term tobacco smoke exposure on whole blood viscosity in the rat.

The purpose of this study was to determine the effect of long-term tobacco smoke administration to rats on whole blood viscosity. Blood samples obtained from rats that had been administered tobacco smoke daily for a period of 10 wk and samples from normal cage control rats were placed in a cone-plate viscometer. Whole blood viscosities were measured at shear rates ranging from 23 to 230/sec. At every shear rate tested, blood viscosity from the smoke-treated animals was significantly higher than corresponding viscosities from the control rats. It is concluded that chronic tobacco smoke administration to rats increases the viscosity of whole blood, both at high shear rates where blood behaves rheologically as a Newtonian fluid and at low shear rates where blood displays non-Newtonian properties.

Animals

[Influence of isoxsuprine HCl on blood viscosity].

A decrease of blood viscosity is a working principle in the therapy of severe disorders of arterial blood flow. Isoxsuprine-HCl was found effective in lowering the blood viscosity when given intravenously in a dose of 30 mg over 60 min. This effect derives probably from a decrease of the tendency to aggregate and an increase of the flexibility of red blood cells. 30 min after termination of the infusion this effect has its maximum and 60 min later still is significantly raised.

Blood Viscosity

Effect of low-dose subcutaneous heparin on whole-blood viscosity.

The change in blood-viscosity at low shear-rates (0.77 s-1 and 2-62 s-1 was measured in eighteen normal subjects and postoperatively in sixteen patients after administration of 5000 I.U. of subcutaneous heparin. In both groups there was a significant decrease in the mean blood-viscosity 4 to 6 hours after the injection of heparin. This fall in blood-viscosity may be involved in the prophylactic effect of low-dose subcutaneous heparin in preventing venous thrombosis.

Blood Viscosity

Changes in blood viscosity and plasma proteins in carcinoma.

Blood viscosity and plasma protein concentrations were measured in 31 patients with a variety of visceral carcinomas. The mean whole blood viscosity was not elevated over normal controls because of a significantly lowered mean hematocrit. However, when hematocrit was eliminated as a variable by adjusting the hematocrit to 45%, the mean whole blood viscosity was significantly elevated in the group with carcinoma. Both the plasma viscosity and the tendency for red cell aggregation were significantly elevated. Since blood is a non-Newtonian fluid, and its viscosity increases markedly at low shear rates, these rheological abnormalities would be most important at the low shear rates characteristic of the venous circulation. It is suggested that these abnormalities in blood viscosity and red cell aggregation may be contributing to the high incidence of venous thromboembolism seen in patients with neoplastic.

Alpha-Globulins

Blood viscosity in Waldenström macroglobulinemia.

Patients with Waldenström macroglobulinemia were studied for the presence or absence of the hyperviscosity syndrome, the relative serum viscosity value, and the calculated whole blood viscosity to identify a level at which symptoms occurred. The majority of symptomatic patients had whole blood viscosity values above 8.0 centipoises. There was a direct correlation between whole blood viscosity and relative serum viscosity, r = 0.75. One patient with central nervous system abnormalities was identified as having a high whole blood viscosity but a low serum viscosity. It was concluded that the vast majority of patients with the hyperviscosity syndrome will be identified by measuring the relative serum viscosity. In patients with central nervous system findings and a low serum viscosity, the whole blood viscosity should be determined either by direct measurement or by calculation.

Blood Viscosity

Blood viscosity and cardiac output in acute experimental anemia.

The significance of blood viscosity alterations during anemia was evaluated in dogs under morphine-chloralose anesthesia. In group I, anemia (mean hematocrit 18.1 +/- 1.3 vol %) was produced by exchange transfusion with clinical dextran (avg mol wt 70,000). In group II, anemia was produced (mean hematocrit 19.9 +/- 0.88 vol %) with 500,000 molecular weight dextran, thus preventing the decrease in blood viscosity in group I. The cardiac output increase in group I (93.4%) with low-viscosity anemia was significantly greater than in group II (43.3%) with unchanged blood viscosity. Group III animals were transfused with a clinical dextran-red cell mixture, and group IV animals received a 500,000 mol wt dextran-red cell mixture. In group III, blood viscosity and cardiac output did not change. In group IV, blood viscosity rose and cardiac output fell significantly. The results suggest that a change in blood viscosity exerts a significant effect upon cardiac output, especially during acute dextran-exchange anemia.

Anemia

Blood viscosity and oral anticoagulant therapy.

During administration of bishydroxycoumarin, hematocrit, viscosity of whole blood, and viscosity of plasma decreased in samples from nine healthy volunteers and 31 patients who had coronary heart disease. The relationships between viscosity of blood and intensity of anticoagulant therapy varied from patient to patient. Discontinuation of the drug was followed by return of viscosities to pretreatment levels in two to four days. The decrease of viscosity of blood by anticoagulant therapy may explain the relief of anginal pain in patients who have coronary heart disease.

Administration, Oral

[Study of blood viscosity for evaluation of peripheral circulation in ischemic heart disease].

An important role in the characterization of the functions of the circulatory system belongs to the interrelationship between blood viscosity and central haemodynamics. Blood viscosity was studied in comparison with the pulse rate, arterial pressure and Robinson's index in patients with chronic forms of ischaemic heart disease. The examinations were conducted at rest and at the peak of sub-maximal bicycle tests. In normal individuals blood viscosity increases along with the increasing workload of the exercise. In patients with ischaemic heart disease performing threshold exercises the shifts in blood viscosity were varidirectional. In patients without circulatory insufficiency blood viscosity was changing in the same way as in normal individuals. In patients with cardiac insufficiency it either remained unchanged, or decreased. An increasing blood viscosity in normals under physical exercises may be interpreted as a mechanism of homeostasis preservation. A lack of growing blood viscosity under threshold exercises in patients with ischaemic heart disease and circulatory insufficiency indicates to disorders in the mechanisms of homeostasis preservation. Increasing blood viscosity may be due to impaired tissue oxygenation.

Adult