Biomedical Engineering Reference
In-Depth Information
the modified surfaces by the SMA-induced albumin selective binding as de-
scribed in Sect. 2.2.2, by this means less fibrin formation is still acquired
eventually [78, 79].
Anti-Haemolysis/Inflammation
Extrinsic thrombosis frequently complicates with haemolytic and inflamma-
tory reactions especially on the interface of interventional materials. Given
the usual risks of these complications, blood cell compatibility of biomaterials
is also considered a significant aspect among the overall haemo-compatibility.
Haemolysis refers to breakage of red blood cells [RBCs], which causes the
release of haemoglobin [HGB] and haemolytic debris that also joins the
construction of the thrombus. The biomaterials invasion-related inflamma-
tions originate from surface infection of pathogenic microorganisms and
the accompanying leucocyte (namely white blood cells [WBCs]) adhesion.
Accordingly, the surface-modifying countermeasure against haemolysis and
infection is to generally minimize the cell-leveled adhesion. On the basis
of the prototype of MPEO-derived SMAs, spatial repulsion and denatura-
tion protection are talents of PEG spacers; while for cell-leveled adsorbing
counterparts, C18 endgroups are unable to directly offer any specific binding
affinity. Therefore, as demonstrated in Fig. 7D, an unsophisticated resistance
is established to both RBC and WBC adhesion on the modified PEsU sur-
faces [78, 79].
2.2.4
Endothelialization
Tissue-engineered strategies engaged with development of blood-contacting
devices are largely represented by surface endothelialization of the employed
biomaterials. The rationale is straightforward. An engineered vascular en-
dothelium offers ideal compatibility when interfacing with blood compo-
nents, hence despite other comprehensive vascular functions and features
such as smooth muscle-related vessel mechanics etc., in vivo renewable en-
dothelialization illuminates the ultimate solution for haemo-compatibility of
synthetic substitutes. The applied cells for transplantation are usually vas-
cular endothelial cells [ECs]. The seeding-to-confluence of ECs on the inner
surface of engineered blood vessels, namely the engineered endothelium, is
capableofisolatingthebloodstreamfromdirectlytouchingthesynthetic
vascular wall that is mostly vulnerable to clotting. Accordingly, a virtual
model of tissue engineered, permanent substitution of blood vessels can be
built up with this strategy—the synthetic outer wall is utilized for suture with
the connective tissue-based native vascular wall at both ends of the substitute;
while the engineered inner endothelium also tends to fuse with the native
endothelium from both sides and eventually achieves a complete confluence
with the native cell populations [30-36].
