This study examined the effects of red blood cell (RBC) aggregation at pathological levels on NO/O2 transport in small arterioles. Transient gas diffusion simulations were performed with in vivo cell-free layer (CFL) widths data obtained from arteriolar flows in the rat cremaster muscle. The CFL data were measured at physiological and pathological levels of aggregation under reduced flow conditions (pseudoshear rate = 31.4 ± 10.5 s-1). Our results showed that the mean peak NO concentration significantly decreased with increasing the aggregation level from non-aggregating to normal-aggregating (P < 0.05) and to hyper-aggregating (P < 0.01) conditions. In contrast, the partial O2 pressure (PO2) in pathological aggregating conditions significantly increased from those under non-aggregating (P < 0.001) and normal-aggregating (P < 0.05) conditions. Although the NO scavenging by RBCs could be impaired with a thicker CFL at higher levels of aggregation, the overall decrease in NO production due to reduction of wall shear stress with the thicker CFL dominantly limited the NO availability in tissue. On the other hand, the O2 availability in tissue increased due to the relatively high core hematocrit in the blood lumen with the thicker CFL.
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)