[Hemorheologic variables in manifest arterial vascular diseases].
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Biomedical subjects
Publications and source records attributed to A Matrai.
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The effects of serotonin and its pharmacological antagonists on the physical flow properties of the blood have been studied far less than their effects on blood vessels, although they may be equally important. Indirect evidence suggests that in pathological circumstances serotonin may locally increase whole blood viscosity, particularly at low shear rates, decrease red cell deformability and increase the adhesiveness of white cells. Although the viscosity of the plasma alone is not affected, the rheological effects of serotonin on blood cells is probably dependent on the presence of platelets. These mechanisms may have a systemic effect in some forms of hypertension as well as in situations of local ischaemia such as Raynaud's phenomenon, atherosclerotic pregangrene of the leg or acute myocardial infarction. Specific serotonergic-antagonists, administered either orally or intravenously, normalize the increased whole blood viscosity and decreased blood filterability found in essential hypertension, following myocardial infarction and in severe leg ischaemia. The effect on red cell deformability is usually greatest when the cells are resuspended in platelet rich plasma. Ketanserin given intravenously for seven days to patients with very severe leg ischaemia, significantly improves whole blood viscosity, increases red cell transit time and most dramatically decreases pore clogging. This last effect was at least partly due to a change in the physical properties, but not the number of the white cells. The reported beneficial clinical effects of such an antagonist in various forms of peripheral ischaemia and essential hypertension may well be due, at least partly, to the normalization of the rheological properties of the blood.
The role of different factors contributing to red cell filterability in the Hemorheometre has been investigated. Although the original method uses a small volume of suspension to determine red cell filterability, the present experiments showed that the results obtained are still significantly affected by filter clogging. Consequently a change in filterability could be due to a change in filter clogging possibly by residual leucocytes. An adaptation of filter chamber and filling method is described, resulting in a simpler and faster measuring procedure. The inaccuracy in measuring low haematocrits contributes significantly to experimental errors. Therefore a definition of red cell filterability based on the red cell count (instead of haematocrit) of the suspension is suggested.
Three rotational viscometers for blood viscometry were compared at moderate and high shear. At high shear, coefficients of variation were all around 1% increasing 5-fold (Wells-Brookfield) and 3-fold (Carri-Med) when shear was lowered. Using pathological samples the coefficients of variation for the Carri Med mashine was doubled. Only the Contraves LS-30 viscometer showed neither an increasing coefficient of variation with declining shear, nor problems when measuring blood with suspension instability.
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Aggregation and sedimentation of the red cells in the viscometer makes it difficult to obtain good reproducibility at low shear rates. A simple method is described to obtain repeatable torque-time curves with the Contraves LS30. Before starting rotation, the blood sample is agitated by an up and down movement of the bob. This results in identical (within 1-2% of the actual amplitude) repeated tracings even at the lowest shear rates, even with extremely time-dependent samples. The subsequent torque-time curve of the disaggregated and unsettled samples provides an experimental basis for the quantitative description of blood viscoelasticity and for dynamic analysis of red cell aggregation: furthermore it results in more accurate measurements when comparing different samples and testing therapeutic effects. The method is applicable to any coaxial cylinder type viscometer with manual lowering of the bob.
The weak interactions between plasma proteins are of possible importance both in haemorheology and in the pathology of several diseases. The use of surface rheology is a convenient way to study the forces arising between surface adsorbed protein molecules. A surface rheological measuring head has been designed for the Contraves LS-30 viscometer. Plasma samples of healthy human subjects showed a rapidly developing viscous surface layer with a mean peak value of 2.10(-3) Ns/m surface viscosity at 30- 60 seconds. After that the viscosity of the surface layer gradually decreased to zero between 8-20 minutes. The rate of the observed decrease was not related to shearing. There was no difference between samples anticoagulated with heparin or EDTA. The time course of the described phenomenon coincides with that of thrombocyte and white cell adherence to solid surfaces exposed to plasma.
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To investigate the relationship between cardiovascular risk factors and the fluidity of blood, a random sample of the population consisting of 4022 persons ages 25 to 64 years was investigated for plasma viscosity, hemoglobin, and total serum protein. A total of 567 healthy nonsmokers and 287 healthy smokers were identified and compared. Plasma viscosity was found to be elevated in male smokers; this was related to both the degree and the duration of cigarette abuse. Plasma viscosity proved to be age-dependent in smokers, but did not change with age in nonsmokers. Total serum protein decreased with age in nonsmokers, while it did not change in smokers. Hemoglobin increased only in female smokers. These findings suggest that blood fluidity is jeopardized in smokers. In men the hemorheological deficit is mostly due to a rise of plasma viscosity, which, in turn, may be caused by an elevation of plasma fibrinogen levels. In women it is predominantly due to an increase in hemoglobin. These alterations in hemorheological variables may be a marker for increased cardiovascular risk in smokers and could reduce blood flow and hinder microcirculatory function.
Eighteen patients with recent ischemic stroke were compared with an equal number of matched controls. Standardized suspensions of red cells as well as of red and white cells were filtered in a new filtration apparatus capable of discriminating between cell deformability and filter occlusion. Results show that red cell deformability, although slightly lower than in controls, is not significantly altered in stroke patients. Filter occlusion, however, was significantly higher in patients when red and white cell suspensions were filtered, but not when red cell suspensions were used, suggesting that white cell filterability is impaired after stroke, which could be due to decreased deformability and/or increased adhesiveness of leukocytes. Slowed white cell passage may also occur in the living microcirculation and may present an obstacle to nutritive flow in exchange vessels, possibly contributing to local ischemia and tissue necrosis after stroke.