Reduction In Blood Viscosity Research Articles

Hyperviscosity syndrome in IgA multiple myeloma.

Summary. Four cases of IgA multiple myeloma with raised serum or Plasma viscosity and clinical features of the hyperviscosity syndrome (HVS) are described. Plasmapheresis was effective in reducing blood viscosity and improving the clinical condition in all four patients. In three of four cases plasma viscosity studies showed an increase in viscosity at low temperature which in one patient was attributable to excess chylomicrons. Although rarely reported in the past, IgA myeloma has been the commonest cause of HVS in Cardiff and should be looked for in all cases of myeloma whatever the paraprotein type. Measurement of serum viscosity is essential for rational clinical management. Whole blood viscosity measurements, although technically more difficult, are also of great help in patient management.

Effect of red cell volume reduction on pulmonary blood flow in polycythemia of cyanotic congenital heart disease

The acute effects of red cell volume reduction (erythropheresis) on pulmonary blood flow and pulmonary vascular resistance were measured in 16 patients with severe shunt-induced polycythemia. In subjects with D-transposition of the great arteries and no significant pulmonary stenosis (Group A) erythropheresis was associated with a decrease in pulmonary vascular resistance and an increase in pulmonary blood flow and in mixing between the systemic and pulmonary circulations. Systemic arterial saturation decreased slightly. By contrast, erythropheresis in patients with severe pulmonary stenosis or atresia and a ventricular septal defect (Group B) was associated with a decrease in pulmonary blood flow and left to right shunt and an increase in right to left shunt. These alterations resulted in a significant reduction in systemic arterial oxygen saturation despite relatively little change in effective pulmonary blood flow. The acute hemodynamic effects of packed red cell transfusion in five patients with D-transposition of the great arteries, no significant pulmonary stenosis and relative anemia were more variable. The observations in patients with shunt-induced polycythemia are probably related to a reduction in blood viscosity produced by a lowering of hematocrit concentration. The reduced viscosity decreases the impedance to flow in the systemic and pulmonary circulations. When pulmonary blood flow is largely derived from the systemic circuit, erythropheresis will diminish pulmonary flow and reduce systemic oxygen saturation. If the pulmonary blood flow is largely independent of the systemic circuit (as in D-transposition of the great arteries without pulmonary stenosis), an increase in total and effective pulmonary flow occurs.

Study on alterations of blood flow and blood viscosity under hemorrhagic shock and effects of plasma expander.

Experiments were performed in 48 dogs subjected to a shock produced by hemorrhage after the modified Wiggers' method. Dogs were infused 90 minutes after hemorrhage with one of six test substances; shed blood, 5% glucose solution, or four kinds of dextran ( mw. 75,000, 47,000, 29,000 and 12,000 ). Infusion of dextran with mw. 29,000 produced the most remarkable increase in femoral arterial blood flow above the prehemorrhagic level. This flow improvement was thought to be more attributable to reduction in blood viscosity than an increase in blood volume. INTRODUCTION The development of shock is a complicated phenomenon not necessarily causally related to any one factor. The shock may be resulted from a multiplicity of influences such as hormonal, neural, circulatory and so onn. Hemorrhage, if it is significant in amount, may cause irreversible responses of the circulatory system. Maintenance of blood volume and blood pressure is necessary, but there is no guarantee to restore capillary circulation even with an adequate blood replacement. The circulatory conditions after hemorrhage are accompanied by cellular aggregation or sludging, increased blood viscosity and venular stasis of cells11 41 • Cellular aggregation, if uncorrected, may reduce nutritive capillary blood flow and result in hypoxic damages of the parenchymatous organs. A failure of capillary circulation is related to a principal cause of a fatal process. Reversal of cellular aggregation with return toward normal circulation is seen after the administration of low molecular weight dextran (LMWD )215)-91. The hemodynamic changes induced by the LMWD administration have been studied, both in terms of acute plasma volume expansion and in terms of blood flow increase attributed to the viscosity altering effects101 131 • Many studies216171 101 121 emphasize the relationship of viscosity alterations to the microcirculatory changes in the disturbed circulatory states and the usefulness of LMWD for Received for publication December 12, 1967. ~7l<rr'frl

Reduction in blood viscosity at low rates of shear by surface active substances: a new hemorheologic phenomenon.

Sodium oleate, representing substances that disrupt erythrocyte aggregates, has been found to considerably decrease the low shear viscosity of blood in optimal concentrations of 20–40 mg per cent. Evidence suggests that this effect is due to reversib

Effects of dextran-40 on blood viscosity in experimental macroglobulinaemia.

BLOOD viscosity may be raised in many diseases. This rise may compromise the perfusion and nutrition of organs throughout the body1–3; therefore there is great interest in any agent capable of reducing blood viscosity. Dextran-40 has been thought to be unique in performing this function3–7, but since its introduction as a plasma expander it has been the object of controversy because of conflicting reports about both its actual effect on viscosity and its mode of action2,3,7–14. Solutions of this type of dextran, with an average molecular weight of 40,000 (also known as low molecular weight dextran8, low viscosity dextran4,5 and ‘Rheomacrodex’6), were said to reduce blood viscosity by inhibiting or reversing the formation of erythrocyte (RBC) aggregates1–7 the presence of which is thought to contribute to the elevated viscosity levels found in pathological states1,2. The evaluation of dextran-40 is complicated, however, by the multiplicity of its effects, and particularly by its ability to expand the volume of plasma and reduce the haematocrit, alterations which in themselves lower blood viscosity1,2,3,4,6–8. Indeed, many investigators have concluded that all the beneficial effects of dextran-40 can be ascribed to blood dilution8,10–14, and evidence has appeared showing that this agent, like dextrans of higher molecular weight, will actually increase blood viscosity if the haematocrit is not permitted to fall3,10,12,15. Nevertheless, some workers still feel that infusions of dextran-40 are of special value in the treatment of hyperviscous states, and that the beneficial effects of this agent are mediated, at least in part, through the dissolution of RBC aggregates7.

Effects of increased osmolality and correction of acidosis on blood flow and oxygen consumption in hemorrhagic shock

Hypertonic NaHCO 3 or NaCl given to an animal in hemorrhagic shock with the blood pressure maintained at the shock level by an open reservoir produced marked increases in cardiac output and oxygen consumption. This occurred in spite of large volumes of blood which were removed to maintain the same low blood pressure and decreased arterial oxygen content. Hematocrit was greatly decreased, which would reduce blood viscosity, and plasma osmolality was increased. The increased survival rate and reduced tissue damage found in other studies with hypertonic infusions during hemorrhagic shock would seem to be the result of this hemodynamic improvement. Cellular overhydration may occur with shock, but because of changes in blood flow and oxygenation, experiments such as this yield no information about the possibility of its occurrence or reversal by increased osmolality. The hemodynamic and oxygenation changes with NaCl and NaHCO 3 in hemorrhagic shock were comparable and indicate that the improvement after NaHCO 3 was due to an osmotic effect rather than to pH correction. This suggests that circulatory depression by metabolic acidosis either was not present at the time and levels studied or could not be separated from the extensive osmotic effects of these solutions.

Blood Viscosity Changes in Acute Myocardial Infarction

Plasma protein changes of acute tissue injury are seen in acute myocardial infarction, and the increase in hematocrit and blood viscosity represents increased strain on the heart. The phenomenon of intravascular sludging will appear, effecting either a temporary drop in viscosity or a more prolonged drop in both viscosity and hematocrit. Improved hydration alone does not reduce viscosity as measured, but dextran of low molecular weight significantly reduces blood viscosity during the period of its administration. This action should materially reduce the work of the heart and, in effect, rest it during this period of acute stress.

Low Molecular Weight Dextran in Treatment of Severe Ischemia

The flow of blood through the microvasculature is as vital to life as that through the heart and great vessels. Roe Wells, Jr. SWEDISH dextran with its molecular weight of 40,000 has been in wide use in situations of easing blood flow. Its properties are quite different from those of its American (weight, 75,000) and British (weight, 150,000) relatives. Principally, it affects a reversal of red cell aggregation and reduces blood viscosity.1Since this results in an increase in tissue perfusion, it has been apparent that theoretically this agent would be useful in treatment of patients with severe ischemia. Several preliminary reports have suggested some improvement of blood flow by dextran in some ischemic states.2-4In others, the nontoxic properties and general safety of the agents has been documented.5,6As a result, it has seen extensive use abroad and in this country in a remarkably diverse group

Dextran-exchange anemia and reduction in blood viscosity in the heart-lung preparation

In dog heart-lung preparations, a 1-liter dextran exchange lowered hematocrits from an average of 53 to 13, with an average increase in cardiac output of 38 per cent, and an in vitro decrease in blood viscosity of 33 per cent. Atrial pressures fell and ventricular force rose. When blood viscosity was reduced without anemia by an exchange of dog red cells suspended in Krebs' solution, there was a similar change in cardiac dynamics. These results suggest that reduced blood viscosity is an important factor in the increased cardiac output of anemia. When hematocrits were lowered to 2 to 7 per cent by further dextran exchange, anemic heart failure resulted, with rising atrial pressures and declining cardiac output. After 375 to 500 μg of ouabain, atrial pressures fell and cardiac output rose in 11 of 12 preparations with anemic heart failure. The anemic heart failure could also be improved or eliminated by restoration of the hematocrit to normal.

THE VISCOSITY OF THE BLOOD IN NARROW CAPILLARY TUBES

THE VISCOSITY OF THE BLOOD IN NARROW CAPILLARY TUBES