The influence of radial RBC distribution, blood velocity profiles, and glycocalyx on coupled NO/O₂ transport

Abstract

The purpose of this investigation was to study the effect of the presence of red blood cells (RBCs) in the plasma layer near the arteriole wall on nitric oxide (NO) and oxygen (O2) transport. To this end, we extended a coupled NO and O2 diffusion-reaction model in the arteriole, developed by our group, to include the effect of the presence of RBCs in the plasma layer and the effect of convection. Two blood flow velocity profiles (plug and parabolic) were tested. The average hematocrit in the bloodstream was assumed to be constant in the central core and decreasing to zero in the boundary layer next to the endothelial surface layer. The effect of the presence or absence of RBCs near the endothelium was studied while varying the endothelial surface layer and boundary layer thickness. With RBCs present in the boundary layer, the model predicts that 1) NO decreases significantly in the endothelium and vascular wall; 2) there is a very small increase in endothelial and vascular wall Po2; 3) scavenging of NO by hemoglobin decreases with increasing thickness of the boundary layer; 4) the shape of the velocity profile influences both NO and Po2 gradients in the bloodstream; and 5) the presence of RBCs in the boundary layer near the endothelium has a much larger effect on NO than on O2 transport.

Nitric oxide transport in an axisymmetric stenosis

“…Owing to the high NO reaction rate by RBCs, the presence of RBCs in the lumen significantly reduced the NO concentration on the endothelium, which has also been demonstrated in the capillaries and arterioles [16,21,37]. However, the effect of RBCs on NO transport in the artery was diminished by the existence of the RBC-free plasma layer at the blood-endothelium interface because of the much lower NO reaction rate in the layer, which was consistent with Liao et al's experiments [36].…”

Vascular and perivascular nitric oxide release and transport: Biochemical pathways of neuronal nitric oxide synthase (NOS1) and endothelial nitric oxide synthase (NOS3)

“…The change in oxygen level results in vasodilation, which increases the blood flow and ensures the delivery of the adequate oxygen to match the tissue's metabolic requirements. Moreover, the transport of oxygen and NO can be coupled and influence each other [52]. With regard to the endocrine vasodilation induced by NO during hypoxia, one of the questions that remains to be elucidated is how the vasculature senses oxygen.…”

The revised World Health Organization diagnostic criteria for polycythemia vera, essential thrombocytosis, and primary myelofibrosis: an alternative proposal

“…Contrary to the WHO claim, the treatment of "high-risk" MPD patients is not the same regardless of diagnosis because there is as yet no drug therapy proven to prevent venous thrombosis in PV [101][102][103][104] (Figure 3), whereas phlebotomy to a sex-specific hematocrit 105 rapidly alleviates the hyperviscosity symptoms unique to PV, as well as reduces the red cell contribution to thrombosis by lowering blood viscosity 46 and diminishing red cell nitric oxide scavenging. 106 Moreover, It would be inappropriate to treat an ET patient for PV; the assumption of PV when that disease was not present has been associated with the iatrogenic induction of acute leukemia. 107,108 …”