Effect Of Blood Viscosity Research Articles

Blood flow and oxygen delivery to the organs of the neonatal lamb as a function of hematocrit.

We chronically catheterized 15 newborn lambs (9.5 +/- 2.8 days) and measured the distribution of cardiac output by the radionuclide-microsphere technique at hematocrits ranging from 10 volumes % to 55 volumes %. Seven animals were made progressively anemic and eight polycythemic by means of exchange transfusions. Cardiac output and heart rate increased with decreasing hematocrit while whole body oxygen consumption showed a small decrease during severe anemia. Both cerebral and cardiac blood flow markedly increased during anemia which assured a relatively stable oxygen delivery to both organs. The changes seen for blood flow to the carcass (skin, bones, and muscle) were predictable from the effects of blood viscosity: small decreases in flow at the highest hematocrits and small increases in flow at the lowest hematocrits. Consequently, oxygen delivery was as low as 1 ml of oxygen/min/100 g at a hematocrit of 10 volumes %. Renal blood flow remained unchanged while oxygen delivery fell when hematocrit was decreased. Hepatic oxygenation was measured using a modification of the Fick principle. Hepatic blood flow showed only a small decrease as hematocrit increased and changed minimally during anemia resulting in a falling delivery of oxygen with anemia. A stable hepatic oxygen consumption was assured by a marked increase in oxygen extraction during anemia. Two differing organ responses to changes in hematocrit can be seen in the newborn: the brain and heart vary blood flow to assure an adequate delivery of oxygen while a number of other organs show less blood flow regulation and, most likely, vary oxygen removal from blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of blood viscosity on plasma renin activity and renal hemodynamics

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

The effect of blood viscosity on blood flow in the experimental saphenous flap model

A study has been made of the effect of lowering blood viscosity with ancrod (Arvin) on blood flow in an experimental island skin flap. Blood flow was measured directly using an electromagnetic flowmeter. It was observed that blood flow into the flap increased significantly (p < 0.02) as a result of lowering blood viscosity.

The effect of blood viscosity on blood flow in the experimental saphenous flap model

The effect of blood viscosity on blood flow in the experimental saphenous flap model

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.

Effect of blood viscosity on pulmonary vascular resistance

In the treatment of congenital cyanotic heart disease, the effectiveness of palliative shunts between the systemic arterial or systemic venous circulation and the pulmonary arterial circulation is dependent in no small part upon resistance to pulmonary blood flow. Factors that increase pulmonary vascular resistance tend to decrease the volume flow to the lungs by way of these shunts, and hence, to decrease their effectiveness. It has long been known that increased blood viscosity increases systemic vascular resistance and, secondarily, decreases total cardiac output in the intact circulation. 1 Similar changes of increased pulmonary vascular resistance have been seen when blood viscosity is increased; but since increased pulmonary vascular resistance occurs in the face of diminished cardiac output for whatever cause, it is not known whether increased blood viscosity is a primary factor in increasing resistance in the pulmonary circulation or if the increased pulmonary vascular resistance observed is a consequence only of diminished cardiac output. Since the functional effectiveness of systemic arterial or venous-pulmonary artery shunts is dependent primarily upon pulmonary vascular resistance, it seems important to determine what effect changes in blood viscosity have on pulmonary vascular resistance independent of changes in cardiac output.

Effects of vasoconstriction on blood viscosity in vivo.

AbstractThe influence of vascular dimensional changes on blood viscosity in vivo (“effective” viscosity) was analyzed in the calf muscle vascular bed of cats. Values for effective blood viscosity over an extensive flow range were obtained from comparisons of pressure‐flow curves for blood and a Newtonian fluid (Dextran‐Tyrode) with known viscosity. Such comparisons were made both at high and low flows during maximal vasodilataion and at low flows during vascular narrowing, caused either by vessel collapse or by intense, stable vasoconstriction as a result of barium chloride infusion. At indentical low flows effective blood viscosity was substantially lower in the constricted or collapsed bed than in the dilated and distended bed. With reduction of flow from maximal to very low values in the completely dilated, non‐collapsed bed effective blood viscosity increased from about 2.35 cP by 200–300 per cent. If the same low flows occurred as a result of intense vasoconstriction, implying a more than 5000 per cent increase of flow resistance, the viscosity increased by about 30 per cent.Apparently, effective blood viscosity is normally low and varies very little within the extensive flow range met with in vivo as a consequence of alterations of vascular tone. Therefore, even at extremely low flows in the constricted bed, as after severe blood loss, effective blood viscosity is hardly a significant determinant of flow, as long as blood composition is not changed.

Effects of blood viscosity on hemodynamic responses in acute normovolemic anemia.

Effects of blood viscosity on hemodynamic responses in acute normovolemic anemia.