Biomedical Engineering Reference
In-Depth Information
Fig. 7 D
Measurements of hemoglobin [HGB] and blood cells including red blood cells
[RBC] and white blood cells [WBC] [78]. Reproduced from [179]
the SMAs, and also involves variables of coating aids, respectively PEU and
chitosan. Physiological-mimicking blood flows are manipulated with a peri-
staltic pump system by which various shear rates are simulated and exerted
to the modified surfaces for a performance testing under dynamic condi-
tions [171, 172].
Resistance of Platelet Adhesion
Platelets, also called thrombocytes, are plasma membrane-possessed mega-
karyocyte fragments that play a pivotal role in blood clotting. Generally,
damage of native vascular endothelium or invasion of foreign materials tends
to activate platelets and thereby lead to platelet adhesion, aggregation, and
release. Platelet behavior largely dominates the entire course of the throm-
bogenic cascade. Initially, the adhesion and aggregation of activated platelets
serves for preliminary haemostasis by producing floppy “sealants”. Platelet
aggregates provide phospholipidic substrates for the activation of bound
coagulation factors (typically clotting Factors V and prothrombin), which
enables the clotting cascade to proceed via a series of catalyzed surface re-
actions. The activated platelets are also capable of releasing thrombogenic
intracellular substances (typically ADP, etc) to further solidify the clot. Ac-
cordingly, in order to pursue haemo-compatible biomaterial surfaces, the
SMAs' primary responsibility is to resist platelet adhesion and simultaneously
minimize the binding of proteinic clotting factors, so as to hinder the throm-
bogenic cascade. As indicated in Fig. 7B, MPEO-derived SMAs function for
minimizing platelet adhesion on the modified PEsU surfaces and the optimal
efficacy is attributed to a proper coordination of SMA spacers with functional
