Influence of acute reduction of blood viscosity on endothelial function

Abstract

BACKGROUND:The relationship between blood viscosity (BV) and endothelial function is rather complex. An increase in BV causes an increase in blood flow resistance, with negative hemodynamic effects; on the other hand, a moderate increase in BV causes an increase in wall stress shear (WSS), and consequent beneficial effects. As a matter of fact, the effect of changes in BV on endothelial function is not yet clear. OBJECTIVES: Aim of the present study was to evaluate in-vivo the effects of the acute reduction in BV on endothelial function, in healthy male subjects. METHODS: Fourteen healthy male blood donors were studied before and 48 hours after blood donation. Blood and plasma viscosity were measured at 37C • with a cone-plate viscometer. Endothelial function was evaluated through flow mediated vasodilation (FMD). RESULTS: Blood viscosity was reduced after blood donation (BV 225 (cP) 4.53 ± 0.59 vs.4.18 ± 0.31, p < 0.05). FMD 50 s after cuff deflation was unchanged: 6.23 ± 3.84 vs. 6.62 ± 4.81, p = NS. The vasodilation, however, lasted longer and the area under the curve of FMD was significantly increased: 8.74 ± 8.77 vs.16.14 ± 8.65, p < 0.005. CONCLUSIONS:The present results demonstrate that the acute reduction of BV prolongs vasodilation, without affecting the amount of vasodilatation, possibly as adaptive reaction allowing more time for oxygen release.

Acute reductions in haematocrit increase flow‐mediated dilatation independent of resting nitric oxide bioavailability in humans

“…Furthermore, it was recently demonstrated that a ∼2% reduction in Hct had no effect on FMD in middle‐aged, overweight individuals without any additional co‐morbidities (Gnasso et al . 2019). Overall, the relatively small changes in Hct/[Hb] and/or presence of co‐morbidities in these latter studies makes reconciliation of these conflicting data problematic.…”

Shear‐thinning behaviour of blood in response to active hyperaemia: Implications for the assessment of arterial shear stress‐mediated dilatation

“…There is evidence from animal models demonstrating that the magnitude of conduit artery dilatation is attenuated in response to a haemodilution‐mediated reduction in blood viscosity via an endothelium shear stress mechanism, independent of alterations of blood flow (Melkumyants & Balashov, ; Melkumyants et al., ). However, it is unclear whether a similar physiological response is evident in humans (Giannattasio, Piperno, Failla, Vergani, & Mancia, ; Gnasso et al., ; Nagy, Toth, Roth, & Tarjan, ; Tremblay et al., ). For instance, using the conventional forearm reactive hyperaemic test, Gnasso et al.…”

“…For instance, using the conventional forearm reactive hyperaemic test, Gnasso et al. () demonstrated that brachial artery dilatation was preserved after a modest decrease in blood viscosity (∼7.7%), via standard blood donation, in middle‐aged healthy men. This result might be explained by the higher shear rate stimulus observed during forearm reactive hyperaemia, thereby counteracting the reduction in blood viscosity (Gnasso et al., ).…”

“…() demonstrated that brachial artery dilatation was preserved after a modest decrease in blood viscosity (∼7.7%), via standard blood donation, in middle‐aged healthy men. This result might be explained by the higher shear rate stimulus observed during forearm reactive hyperaemia, thereby counteracting the reduction in blood viscosity (Gnasso et al., ). Other invasive experimental interventions that acutely manipulate haematocrit (polycythaemia and isovolaemic haemodilution) in patient populations with haematology disorders have yielded equivocal results with respect to the role of blood viscosity in shear stress‐mediated brachial and radial artery dilatation (Giannattasio et al., ; Nagy et al., ; Tremblay et al., ).…”

“…This uncertainty arises from the fact that researchers either ignore or assess blood viscosity in vitro at a single arbitrary shear rate that is different from that in the conduit artery (e.g. Gnasso et al., , ; Joannides et al., ; Parkhurst et al., ; Slattery, Stuckless, King, & Pyke, ; Tremblay et al., ,b).…”