Effects of red blood cell aggregation, hematocrit and tube diameter on wall shear stress in microtubes

Abstract

Wall shear stress (WSS), a tangential stress exerting on the inner surface of blood vessels is an important determinant of endothelial cell structure and function. It is also one of the major stimuli for the release of vasoactive substance, nitric oxide (NO), which plays a critical role in the regulation of vascular diameter and maintenance of vascular resistance. Abnormally low WSS is found to be associated with atherosclerosis whereas abnormally high WSS is correlated with aneurysm. Therefore the study of WSS is of particular importance as any disruptions of WSS in microcirculation might lead to diseases. Red blood cell (RBC) aggregation and hematocrit (Hct) are the main hemorheological factors and contributors to the blood viscosity and vascular resistance. However, little quantitative information of RBC aggregation and Hct on WSS is available. The objectives of the project are to investigate effects of two hemorheological factors RBC aggregation and Hct, and a geometric factor, tube diameter (tube size) on WSS. The study was performed with special reference to the levels of RBC aggregation and Hct found in normal and diseases states in microtubes of inner diameter (ID) 30 µm, 50 µm and 100 µm relevant to microcirculation. Non-aggregating medium of phosphate buffer saline (PBS), normal aggregating medium (Dextran 500-PBS solution of concentration 7.5 mg/ml) and disease aggregating medium (Dextran 500-PBS solution of concentration 12.5 mg/ml) were used in the study. Blood samples at Hct level of 40% mimicking physiological conditions and Hct level of 20% and 60% mimicking clinical levels were utilized. Relative WSS (WSS of blood suspension normalized by the WSS of suspending medium) was used to isolate the medium viscosity effect on the WSS. The results showed that RBC aggregation was effective in reducing the WSS in low pseudoshear rates corresponding to venular flows, but insignificant in affecting WSS in high pseudoshear rates corresponding to arteriolar flows. However, increased Hct and tube diameter led to significant elevations in WSS in most pseudoshear rates except at pseudoshear rate of about 3 s-1 corresponding to reduced venular flows. At low pseudoshear rate of approximate 3 s-1, insignificance difference in WSS between Hct 20% and 40% and between microtubes of ID 30 µm and 50 µm was found in aggregating mediums and this could likely be attributed to the enhanced cell-free layer formation. The results suggested that effects of RBC aggregation could likely be more dominant over effects of Hct and tube diameter in contributing to WSS at low pseudoshear rates whereas the effects of Hct and tube diameter might be more prominent at high pseudoshear rates. The comprehensive quantitative information on effects of RBC aggregation, Hct and tube diameter on WSS with special reference to normal and disease level of RBC aggregation and Hct obtained from the study would lead to an advanced understanding of WSS in vivo and possibly to new therapeutic approaches to the WSS related diseases.