Cardiovascular benefits in moderate increases of blood and plasma viscosity surpass those associated with lowering viscosity: Experimental and clinical evidence

Abstract

Decreasing blood viscosity has been proposed since the advent of hemodilution as a means for increasing perfusion in many pathological conditions, and increased plasma viscosity is associated with the presence of pathological conditions. However, experimental studies show that microvascular functions as represented by functional capillary density in conditions of significantly decreased viscosity is impaired, a problem corrected by increasing plasma and blood viscosity. Blood viscosity, primarily dependent on hematocrit (Hct) is a determinant of peripheral vascular resistance, and therefore blood pressure. In the healthy population Hct presents a variability, which is not reflected by the variability of blood pressure. This is due to a regulatory process at the level of the endothelium, whereby the increase of Hct (and therefore blood viscosity) leads to increased shear stress and the production of the vasodilator nitric oxide (NO), a finding supported by experimental studies showing that the acute increase of Hct lowers blood pressure. Studies that in the healthy population show that blood pressure and Hct have a weak positive correlation. However, when the effect of blood viscosity is factored out, blood pressure and Hct are negatively and significantly correlated, indicating that as blood viscosity increases, the circulation dilates. Conversely, lower Hct and blood viscosity conditions lead to a constricted circulation, associated with a condition of decreased NO bioavailability, and therefore a pro-inflammatory condition.

Blood pressure and blood viscosity are not correlated in normal healthy subjects

“…This result is consistent with the findings of de Simone et al8 who found a negative correlation between the Hct and blood viscosity and pulse pressure in a population of American Indians 62 ± 7 years of age without prevalent cardiovascular disease or use of antihypertensive medications, digoxin, or aspirin. In a study of 128 normotensive members of a large employed population in New York City (51 ± 10 years) there was a significant independent relation between MAP and blood viscosity,9 and a study of 628 individuals in the population of Victoria de Durango with men and women pooled data showed a weak positive correlation between MAP and Hct 10. Our findings and some11,12 but not all results in the literature13,14 support the contention that Hct and blood viscosity are not a factor in regulating blood pressure in the healthy normal population within limits that include the systematic elevation of Hct due to adaptation to moderate altitude.…”

Posttransfusion Increase of Hematocrit per se Does Not Improve Circulatory Oxygen Delivery due to Increased Blood Viscosity

“…As this finding is not consistent with clinical practice, we hypothesize the existence of mechanisms not addressed in our model that ultimately negate the effect of increasing viscosity on blood flow and facilitate DO 2 . One possibility is the decrease of TPR through vasodilatation, which may be mediated by increased mechanotransduction and production of nitric oxide 32, 33,34 . However, in these studies changes in Hct were induced without changes in volume.…”

Asymmetric dimethylarginine and whole blood viscosity in renal failure

“…Our primary goal was to test the claim that ADMA release might be regulated in the same manner as NO: via increase in wall shear stress [25]. As a proxy for wall shear stress, we used WBV which has been thoroughly tested for use in this manner [9].…”